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  • Articles  (121)
  • Latest Papers from Table of Contents or Articles in Press  (121)
  • Signal Transduction  (82)
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  • 1
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    Nuclear accumulation of NFAT4 opposed by the JNK signal transduction pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: The nuclear factor of activated T cells (NFAT) group of transcription factors is retained in the cytoplasm of quiescent cells. NFAT activation is mediated in part by induced nuclear import. This process requires calcium-dependent dephosphorylation of NFAT caused by the phosphatase calcineurin. The c-Jun amino-terminal kinase (JNK) phosphorylates NFAT4 on two sites. Mutational removal of the JNK phosphorylation sites caused constitutive nuclear localization of NFAT4. In contrast, JNK activation in calcineurin-stimulated cells caused nuclear exclusion of NFAT4. These findings show that the nuclear accumulation of NFAT4 promoted by calcineurin is opposed by the JNK signal transduction pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chow, C W -- Rincon, M -- Cavanagh, J -- Dickens, M -- Davis, R J -- CA58396/CA/NCI NIH HHS/ -- CA65831/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1638-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374467" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; COS Cells ; Calcineurin/metabolism ; Calcineurin Inhibitors ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Cyclosporine/pharmacology ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; Jurkat Cells ; Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Mutation ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphorylation ; Protein Kinases/metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; T-Lymphocytes/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    PtdIns(3,4,5)P3 gets its message across (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hemmings, B A -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):534.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute, CH-4002 Basel, Switzerland. hemmings@fmi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9254423" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Enzyme Activation ; Phosphatidylinositol Phosphates/*metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-akt ; Second Messenger Systems ; Signal Transduction
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  • 3
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    Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Integrating genetic approaches into the discovery of anticancer drugs (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-14
    Description: The discovery of anticancer drugs is now driven by the numerous molecular alterations identified in tumor cells over the past decade. To exploit these alterations, it is necessary to understand how they define a molecular context that allows increased sensitivity to particular compounds. Traditional genetic approaches together with the new wealth of genomic information for both human and model organisms open up strategies by which drugs can be profiled for their ability to selectively kill cells in a molecular context that matches those found in tumors. Similarly, it may be possible to identify and validate new targets for drugs that would selectively kill tumor cells with a particular molecular context. This article outlines some of the ways that yeast genetics can be used to streamline anticancer drug discovery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hartwell, L H -- Szankasi, P -- Roberts, C J -- Murray, A W -- Friend, S H -- N01-BC65017/BC/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1064-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Project, Molecular Pharmacology Department, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents/pharmacology/therapeutic use ; *Drug Design ; *Drug Screening Assays, Antitumor ; Humans ; Mutation ; Neoplasms/*drug therapy/genetics ; Signal Transduction ; Yeasts/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Osmotic activation of the HOG MAPK pathway via Ste11p MAPKKK: scaffold role of Pbs2p MAPKK (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: Exposure of the yeast Saccharomyces cerevisiae to high extracellular osmolarity induces the Sln1p-Ypd1p-Ssk1p two-component osmosensor to activate a mitogen-activated protein (MAP) kinase cascade composed of the Ssk2p and Ssk22p MAP kinase kinase kinases (MAPKKKs), the Pbs2p MAPKK, and the Hog1p MAPK. A second osmosensor, Sho1p, also activated Pbs2p and Hog1p, but did so through the Ste11p MAPKKK. Although Ste11p also participates in the mating pheromone-responsive MAPK cascade, there was no detectable cross talk between these two pathways. The MAPKK Pbs2p bound to the Sho1p osmosensor, the MAPKKK Ste11p, and the MAPK Hog1p. Thus, Pbs2p may serve as a scaffold protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Posas, F -- Saito, H -- GM50909/GM/NIGMS NIH HHS/ -- GM53415/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1702-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180081" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Enzyme Activation ; Genes, Fungal ; Genetic Complementation Test ; MAP Kinase Kinase Kinases ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Mutation ; Osmolar Concentration ; Osmotic Pressure ; Peptides/metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/*enzymology/genetics ; *Saccharomyces cerevisiae Proteins ; Signal Transduction
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  • 6
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    Rescue of a Drosophila NF1 mutant phenotype by protein kinase A (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: The neurofibromatosis type 1 (NF1) tumor suppressor protein is thought to restrict cell proliferation by functioning as a Ras-specific guanosine triphosphatase-activating protein. However, Drosophila homozygous for null mutations of an NF1 homolog showed no obvious signs of perturbed Ras1-mediated signaling. Loss of NF1 resulted in a reduction in size of larvae, pupae, and adults. This size defect was not modified by manipulating Ras1 signaling but was restored by expression of activated adenosine 3', 5'-monophosphate-dependent protein kinase (PKA). Thus, NF1 and PKA appear to interact in a pathway that controls the overall growth of Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉The, I -- Hannigan, G E -- Cowley, G S -- Reginald, S -- Zhong, Y -- Gusella, J F -- Hariharan, I K -- Bernards, A -- NS22229/NS/NINDS NIH HHS/ -- NS34779/NS/NINDS NIH HHS/ -- NS36084/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 May 2;276(5313):791-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Harvard Medical School Building 149, 13th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115203" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Count ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/genetics/*metabolism ; Drosophila/cytology/*genetics/growth & development/metabolism ; *Drosophila Proteins ; GTP Phosphohydrolases/metabolism ; Genes, Insect ; Insect Proteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; *Nerve Tissue Proteins ; Neurofibromin 1 ; Phenotype ; Proteins/chemistry/genetics ; Recombinant Fusion Proteins/pharmacology ; Signal Transduction ; *ras GTPase-Activating Proteins ; ras Proteins/metabolism
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  • 7
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    Fluorescence-based isolation of bacterial genes expressed within host cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: A selection strategy was devised to identify bacterial genes preferentially expressed when a bacterium associates with its host cell. Fourteen Salmonella typhimurium genes, which were under the control of at least four independent regulatory circuits, were identified to be selectively induced in host macrophages. Four genes encode virulence factors, including a component of a type III secretory apparatus. This selection methodology should be generally applicable to the identification of genes from pathogenic organisms that are induced upon association with host cells or tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valdivia, R H -- Falkow, S -- AI26195/AI/NIAID NIH HHS/ -- DK38707/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. valdivia@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302299" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics ; Cell Line ; Cloning, Molecular ; Female ; Flow Cytometry ; Fluorescence ; *Gene Expression Regulation, Bacterial ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Luminescent Proteins/genetics ; Macrophages/*microbiology ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Molecular Sequence Data ; Open Reading Frames ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/isolation & purification/*pathogenicity ; Spleen/microbiology ; Transcription Factors/genetics ; Virulence/genetics
    Print ISSN: 0036-8075
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  • 8
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    Formation of actin stress fibers and focal adhesions enhanced by Rho-kinase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-28
    Description: The small guanosine triphosphatase (GTPase) Rho is implicated in the formation of stress fibers and focal adhesions in fibroblasts stimulated by extracellular signals such as lysophosphatidic acid (LPA). Rho-kinase is activated by Rho and may mediate some biological effects of Rho. Microinjection of the catalytic domain of Rho-kinase into serum-starved Swiss 3T3 cells induced the formation of stress fibers and focal adhesions, whereas microinjection of the inactive catalytic domain, the Rho-binding domain, or the pleckstrin-homology domain inhibited the LPA-induced formation of stress fibers and focal adhesions. Thus, Rho-kinase appears to mediate signals from Rho and to induce the formation of stress fibers and focal adhesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amano, M -- Chihara, K -- Kimura, K -- Fukata, Y -- Nakamura, N -- Matsuura, Y -- Kaibuchi, K -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-01, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036856" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/*metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; *Cell Adhesion ; Cell Line ; DNA, Complementary/genetics ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/metabolism ; Intracellular Signaling Peptides and Proteins ; Lysophospholipids/pharmacology ; Mice ; Mutation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Staurosporine/pharmacology ; rho-Associated Kinases
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  • 9
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    Dictyostelium development in the absence of cAMP (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: Adenosine 3',5'-monophosphate (cAMP) and cAMP-dependent protein kinase (PKA) are regulators of development in many organisms. Dictyostelium uses cAMP as an extracellular chemoattractant and as an intracellular signal for differentiation. Cells that are mutant in adenylyl cyclase do not develop. Moderate expression of the catalytic subunit of PKA in adenylyl cyclase-null cells led to near-normal development without detectable accumulation of cAMP. These results suggest that all intracellular cAMP signaling is effected through PKA and that signals other than extracellular cAMP coordinate morphogenesis in Dictyostelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, B -- Kuspa, A -- R01 GM052359/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):251-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Marrs McLean Department of Biochemistry, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211856" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Cloning, Molecular ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Dictyostelium/genetics/*growth & development/metabolism ; Enzyme Activation ; Gene Expression Regulation ; Genes, Protozoan ; Morphogenesis ; Signal Transduction ; Transformation, Genetic
    Print ISSN: 0036-8075
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  • 10
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    Requirement of guanosine triphosphate-bound ran for signal-mediated nuclear protein export (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: A leucine-rich nuclear export signal (NES) allows rapid export of proteins from cell nuclei. Microinjection studies revealed a role for the guanosine triphosphatase (GTPase) Ran in NES-mediated export. Nuclear injection of a Ran mutant (Thr24 --〉 Asn) blocked protein export but not import, whereas depletion of the Ran nucleotide exchange factor RCC1 blocked protein import but not export. However, injection of Ran GTPase-activating protein (RanGAP) into RCC1-depleted cell nuclei inhibited export. Coinjection with Ran mutants insensitive to RanGAP prevented this inhibition. Therefore, NES-mediated protein export appears to require a Ran-GTP complex but does not require Ran-dependent GTP hydrolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richards, S A -- Carey, K L -- Macara, I G -- EST3207122/ES/NIEHS NIH HHS/ -- GM 50526/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1842-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Vermont, Burlington, VT 05405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Carrier Proteins/metabolism ; *Cell Cycle Proteins ; Cell Line ; Cell Nucleus/*metabolism ; Cricetinae ; Cytoplasm ; DNA-Binding Proteins/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/metabolism ; *GTPase-Activating Proteins ; Glutathione Transferase/metabolism ; Green Fluorescent Proteins ; *Guanine Nucleotide Exchange Factors ; Guanosine Triphosphate/*metabolism ; Luminescent Proteins/metabolism ; Mutation ; Nuclear Envelope/metabolism ; Nuclear Localization Signals ; Nuclear Proteins/genetics/*metabolism ; Receptors, Glucocorticoid/metabolism ; Recombinant Fusion Proteins/metabolism ; Temperature ; ran GTP-Binding Protein
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  • 11
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    Neurospora wc-1 and wc-2: transcription, photoresponses, and the origins of circadian rhythmicity (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: Circadian rhythmicity is universally associated with the ability to perceive light, and the oscillators ("clocks") giving rise to these rhythms, which are feedback loops based on transcription and translation, are reset by light. Although such loops must contain elements of positive and negative regulation, the clock genes analyzed to date-frq in Neurospora and per and tim in Drosophila-are associated only with negative feedback and their biochemical functions are largely inferred. The white collar-1 and white collar-2 genes, both global regulators of photoresponses in Neurospora, encode DNA binding proteins that contain PAS domains and are believed to act as transcriptional activators. Data shown here suggest that wc-1 is a clock-associated gene and wc-2 is a clock component; both play essential roles in the assembly or operation of the Neurospora circadian oscillator. Thus DNA binding and transcriptional activation can now be associated with a clock gene that may provide a positive element in the feedback loop. In addition, similarities between the PAS-domain regions of molecules involved in light perception and circadian rhythmicity in several organisms suggest an evolutionary link between ancient photoreceptor proteins and more modern proteins required for circadian oscillation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crosthwaite, S K -- Dunlap, J C -- Loros, J J -- GM 34985/GM/NIGMS NIH HHS/ -- MH01186/MH/NIMH NIH HHS/ -- MH44651/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 May 2;276(5313):763-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Dartmouth Medical School, Hanover, NH 03755-3844, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115195" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Clocks/physiology ; Biological Evolution ; Circadian Rhythm/*physiology ; DNA, Fungal/metabolism ; DNA-Binding Proteins/chemistry/genetics/*physiology ; Feedback ; Fungal Proteins/genetics ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Light ; Molecular Sequence Data ; Neurospora crassa/genetics/*physiology ; Phytochrome/metabolism ; Signal Transduction ; Temperature ; Transcription Factors/chemistry/genetics/*physiology ; *Transcriptional Activation
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  • 12
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    Peptide agonist of the thrombopoietin receptor as potent as the natural cytokine (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: Two families of small peptides that bind to the human thrombopoietin receptor and compete with the binding of the natural ligand thrombopoietin (TPO) were identified from recombinant peptide libraries. The sequences of these peptides were not found in the primary sequence of TPO. Screening libraries of variants of one of these families under affinity-selective conditions yielded a 14-amino acid peptide (Ile-Glu-Gly-Pro-Thr-Leu-Arg-Gln-Trp-Leu-Ala-Ala-Arg-Ala) with high affinity (dissociation constant approximately 2 nanomolar) that stimulates the proliferation of a TPO-responsive Ba/F3 cell line with a median effective concentration (EC50) of 400 nanomolar. Dimerization of this peptide by a carboxyl-terminal linkage to a lysine branch produced a compound with an EC50 of 100 picomolar, which was equipotent to the 332-amino acid natural cytokine in cell-based assays. The peptide dimer also stimulated the in vitro proliferation and maturation of megakaryocytes from human bone marrow cells and promoted an increase in platelet count when administered to normal mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cwirla, S E -- Balasubramanian, P -- Duffin, D J -- Wagstrom, C R -- Gates, C M -- Singer, S C -- Davis, A M -- Tansik, R L -- Mattheakis, L C -- Boytos, C M -- Schatz, P J -- Baccanari, D P -- Wrighton, N C -- Barrett, R W -- Dower, W J -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1696-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Affymax Research Institute, 4001 Miranda Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180079" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Blood Platelets/cytology ; Cell Division ; Cell Line ; Cells, Cultured ; Consensus Sequence ; Dimerization ; Erythropoietin/pharmacology ; Hematopoiesis/drug effects ; Humans ; Megakaryocytes/cytology ; Mice ; Molecular Sequence Data ; *Neoplasm Proteins ; Oligopeptides/*metabolism/*pharmacology ; Peptide Library ; Peptides/metabolism/pharmacology ; Platelet Count ; Proto-Oncogene Proteins/*agonists/metabolism ; *Receptors, Cytokine ; Receptors, Thrombopoietin ; Recombinant Proteins/metabolism/pharmacology ; Thrombopoietin/*metabolism/pharmacology ; Transfection
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  • 13
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    Reduced ubiquitin-dependent degradation of c-Jun after phosphorylation by MAP kinases (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-17
    Description: The proto-oncogene-encoded transcription factor c-Jun activates genes in response to a number of inducers that act through mitogen-activated protein kinase (MAPK) signal transduction pathways. The activation of c-Jun after phosphorylation by MAPK is accompanied by a reduction in c-Jun ubiquitination and consequent stabilization of the protein. These results illustrate the relevance of regulated protein degradation in the signal-dependent control of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Musti, A M -- Treier, M -- Bohmann, D -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):400-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994040" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Cycle Proteins/metabolism ; GTP-Binding Proteins/metabolism ; Gene Expression Regulation ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Phosphorylation ; Proto-Oncogene Proteins c-jun/*metabolism ; Signal Transduction ; Transfection ; Ubiquitins/*metabolism ; cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
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  • 14
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    Interaction and regulation of subcellular localization of CED-4 by CED-9 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: The Caenorhabditis elegans survival gene ced-9 regulates ced-4 activity and inhibits cell death, but the mechanism by which this occurs is unknown. Through a genetic screen for CED-4-binding proteins, CED-9 was identified as an interacting partner of CED-4. CED-9, but not loss-of-function mutants, associated specifically with CED-4 in yeast or mammalian cells. The CED-9 protein localized primarily to intracellular membranes and the perinuclear region, whereas CED-4 was distributed in the cytosol. Expression of CED-9, but not a mutant lacking the carboxy-terminal hydrophobic domain, targeted CED-4 from the cytosol to intracellular membranes in mammalian cells. Thus, the actions of CED-4 and CED-9 are directly linked, which could provide the basis for the regulation of programmed cell death in C. elegans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, D -- Wallen, H D -- Nunez, G -- CA-64556/CA/NCI NIH HHS/ -- T32A107413-03/PHS HHS/ -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1126-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027313" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caenorhabditis elegans/*cytology/genetics ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/analysis/genetics/*metabolism ; Cell Fractionation ; Cell Line ; Cytosol/chemistry ; Genes, Helminth ; Helminth Proteins/analysis/genetics/*metabolism ; Humans ; Intracellular Membranes/chemistry ; Mutation ; Proto-Oncogene Proteins/analysis/genetics/*metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Transfection ; bcl-X Protein
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: Long-term potentiation (LTP), a cellular model of learning and memory, requires calcium-dependent protein kinases. Induction of LTP increased the phosphorus-32 labeling of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPA-Rs), which mediate rapid excitatory synaptic transmission. This AMPA-R phosphorylation appeared to be catalyzed by Ca2+- and calmodulin-dependent protein kinase II (CaM-KII): (i) it correlated with the activation and autophosphorylation of CaM-KII, (ii) it was blocked by the CaM-KII inhibitor KN-62, and (iii) its phosphorus-32 peptide map was the same as that of GluR1 coexpressed with activated CaM-KII in HEK-293 cells. This covalent modulation of AMPA-Rs in LTP provides a postsynaptic molecular mechanism for synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barria, A -- Muller, D -- Derkach, V -- Griffith, L C -- Soderling, T R -- NS27037/NS/NINDS NIH HHS/ -- R01 GM054408/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197267" target="_blank"〉PubMed〈/a〉
    Keywords: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives/pharmacology ; 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Line ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Hippocampus/*metabolism ; Humans ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Male ; Peptide Mapping ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Synaptic Transmission/drug effects
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  • 16
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    Telomerase catalytic subunit homologs from fission yeast and human (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-15
    Description: Catalytic protein subunits of telomerase from the ciliate Euplotes aediculatus and the yeast Saccharomyces cerevisiae contain reverse transcriptase motifs. Here the homologous genes from the fission yeast Schizosaccharomyces pombe and human are identified. Disruption of the S. pombe gene resulted in telomere shortening and senescence, and expression of mRNA from the human gene correlated with telomerase activity in cell lines. Sequence comparisons placed the telomerase proteins in the reverse transcriptase family but revealed hallmarks that distinguish them from retroviral and retrotransposon relatives. Thus, the proposed telomerase catalytic subunits are phylogenetically conserved and represent a deep branch in the evolution of reverse transcriptases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, T M -- Morin, G B -- Chapman, K B -- Weinrich, S L -- Andrews, W H -- Lingner, J -- Harley, C B -- Cech, T R -- GM28039/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):955-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO 80309-0215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252327" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Catalysis ; Cell Line ; DNA-Binding Proteins ; Evolution, Molecular ; Genes, Fungal ; Humans ; Introns ; Molecular Sequence Data ; Phylogeny ; Proteins/*chemistry/genetics/metabolism ; *Rna ; RNA, Messenger/genetics/metabolism ; RNA-Directed DNA Polymerase/chemistry ; Retroelements ; Schizosaccharomyces/*enzymology/genetics/growth & development ; Schizosaccharomyces pombe Proteins ; Sequence Alignment ; Telomerase/*chemistry/genetics/metabolism ; Telomere/metabolism
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  • 17
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    Does a common virus give HIV a helping hand? (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1794.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206839" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/virology ; Cell Fusion ; Cell Line ; Chemokines ; Cytomegalovirus/*physiology ; HIV/*physiology ; Humans ; Receptors, CCR2 ; *Receptors, Chemokine ; Receptors, Cytokine/genetics/*physiology ; Receptors, HIV/*physiology ; Viral Proteins/*physiology
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  • 18
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    Exploitation of mammalian host cell functions by bacterial pathogens (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: Interest in bacterial pathogenesis has recently increased because of antibiotic resistance, the emergence of new pathogens and the resurgence of old ones, and the lack of effective therapeutics. The molecular and cellular mechanisms of microbial pathogenesis are currently being defined, with precise knowledge of both the common strategies used by multiple pathogenic bacteria and the unique tactics evolved by individual species to help establish infection. What is emerging is a new appreciation of how bacterial pathogens interact with host cells. Many host cell functions, including signal transduction pathways, cytoskeletal rearrangements, and vacuolar trafficking, are exploited, and these are the focus of this review. A bonus of this work is that bacterial virulence factors are providing new tools to study various aspects of mammalian cell functions, in addition to mechanisms of bacterial disease. Together these developments may lead to new therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finlay, B B -- Cossart, P -- New York, N.Y. -- Science. 1997 May 2;276(5313):718-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Laboratory, University of British Columbia, Vancouver, B.C., Canada, V6T-1Z3. bfinlay@unixg.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bacteria/genetics/*pathogenicity ; *Bacterial Adhesion ; Bacterial Infections/*microbiology ; Bacterial Physiological Phenomena ; Bacterial Toxins/toxicity ; Cells, Cultured ; Cytoskeleton/physiology ; Epithelial Cells ; Epithelium/microbiology ; Humans ; Phagocytosis ; Signal Transduction ; Vacuoles/microbiology ; Virulence/genetics
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  • 19
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    Conservation of the Chk1 checkpoint pathway in mammals: linkage of DNA damage to Cdk regulation through Cdc25 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: In response to DNA damage, mammalian cells prevent cell cycle progression through the control of critical cell cycle regulators. A human gene was identified that encodes the protein Chk1, a homolog of the Schizosaccharomyces pombe Chk1 protein kinase, which is required for the DNA damage checkpoint. Human Chk1 protein was modified in response to DNA damage. In vitro Chk1 bound to and phosphorylated the dual-specificity protein phosphatases Cdc25A, Cdc25B, and Cdc25C, which control cell cycle transitions by dephosphorylating cyclin-dependent kinases. Chk1 phosphorylates Cdc25C on serine-216. As shown in an accompanying paper by Peng et al. in this issue, serine-216 phosphorylation creates a binding site for 14-3-3 protein and inhibits function of the phosphatase. These results suggest a model whereby in response to DNA damage, Chk1 phosphorylates and inhibits Cdc25C, thus preventing activation of the Cdc2-cyclin B complex and mitotic entry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Y -- Wong, C -- Thoma, R S -- Richman, R -- Wu, Z -- Piwnica-Worms, H -- Elledge, S J -- GM17763/GM/NIGMS NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1497-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Marrs McLean Department of Biochemistry, Howard Hughes Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278511" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Sequence ; Animals ; CDC2 Protein Kinase/*metabolism ; Cell Cycle Proteins/antagonists & inhibitors/*metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Cytoskeletal Proteins ; *DNA Damage ; *F-Box Proteins ; G2 Phase ; HeLa Cells ; Humans ; Mice ; *Mitosis ; Molecular Sequence Data ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Tyrosine Phosphatases/metabolism ; Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Schizosaccharomyces pombe Proteins ; Signal Transduction ; Transfection ; *Tyrosine 3-Monooxygenase ; *Ubiquitin-Protein Ligases ; *cdc25 Phosphatases
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  • 20
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    Caspase-3-generated fragment of gelsolin: effector of morphological change in apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: The caspase-3 (CPP32, apopain, YAMA) family of cysteinyl proteases has been implicated as key mediators of apoptosis in mammalian cells. Gelsolin was identified as a substrate for caspase-3 by screening the translation products of small complementary DNA pools for sensitivity to cleavage by caspase-3. Gelsolin was cleaved in vivo in a caspase-dependent manner in cells stimulated by Fas. Caspase-cleaved gelsolin severed actin filaments in vitro in a Ca2+-independent manner. Expression of the gelsolin cleavage product in multiple cell types caused the cells to round up, detach from the plate, and undergo nuclear fragmentation. Neutrophils isolated from mice lacking gelsolin had delayed onset of both blebbing and DNA fragmentation, following apoptosis induction, compared with wild-type neutrophils. Thus, cleaved gelsolin may be one physiological effector of morphologic change during apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kothakota, S -- Azuma, T -- Reinhard, C -- Klippel, A -- Tang, J -- Chu, K -- McGarry, T J -- Kirschner, M W -- Koths, K -- Kwiatkowski, D J -- Williams, L T -- P01 HL48743/HL/NHLBI NIH HHS/ -- R01 HL54188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):294-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323209" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Antigens, CD95/physiology ; *Apoptosis ; Caspase 3 ; *Caspases ; Cell Line ; *Cell Size ; Cycloheximide/pharmacology ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeleton/metabolism ; DNA Fragmentation ; Gelsolin/*metabolism ; Humans ; Mice ; Neutrophils/cytology/metabolism ; Recombinant Proteins/metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    A cell growth switch (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1891.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206844" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/metabolism ; *Cell Division ; Cell Line ; DNA-Binding Proteins/metabolism ; Dimerization ; Erythropoietin/metabolism ; Heat-Shock Proteins/metabolism ; Humans ; Receptors, Erythropoietin/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Tacrolimus/*analogs & derivatives/pharmacology ; Tacrolimus Binding Proteins
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  • 22
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    Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-06
    Description: Expression of Agouti protein is normally limited to the skin where it affects pigmentation, but ubiquitous expression causes obesity. An expressed sequence tag was identified that encodes Agouti-related protein, whose RNA is normally expressed in the hypothalamus and whose levels were increased eightfold in ob/ob mice. Recombinant Agouti-related protein was a potent, selective antagonist of Mc3r and Mc4r, melanocortin receptor subtypes implicated in weight regulation. Ubiquitous expression of human AGRP complementary DNA in transgenic mice caused obesity without altering pigmentation. Thus, Agouti-related protein is a neuropeptide implicated in the normal control of body weight downstream of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ollmann, M M -- Wilson, B D -- Yang, Y K -- Kerns, J A -- Chen, Y -- Gantz, I -- Barsh, G S -- EY07106/EY/NEI NIH HHS/ -- GM07365/GM/NIGMS NIH HHS/ -- P30DK-34933/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):135-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311920" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Amino Acid Sequence ; Animals ; Female ; Humans ; Hypothalamus/metabolism ; Male ; Melanocyte-Stimulating Hormones/antagonists & inhibitors/pharmacology ; Melanophores/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Obese ; Mice, Transgenic ; Molecular Sequence Data ; Obesity/etiology ; Organophosphorus Compounds/pharmacology ; Proteins/chemistry/genetics/pharmacology/*physiology ; RNA/genetics/metabolism ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Receptors, Corticotropin/*antagonists & inhibitors/metabolism ; Receptors, Peptide/*antagonists & inhibitors/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Xenopus
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  • 23
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    Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC-/- colon carcinoma (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-21
    Description: The adenomatous polyposis coli (APC) tumor suppressor protein binds to beta-catenin, a protein recently shown to interact with Tcf and Lef transcription factors. The gene encoding hTcf-4, a Tcf family member that is expressed in colonic epithelium, was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta-catenin. Nuclei of APC-/- colon carcinoma cells were found to contain a stable beta-catenin-hTcf-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta-catenin from hTcf-4 and abrogated the transcriptional transactivation. Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korinek, V -- Barker, N -- Morin, P J -- van Wichen, D -- de Weger, R -- Kinzler, K W -- Vogelstein, B -- Clevers, H -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065401" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; Colon/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Molecular Sequence Data ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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  • 24
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    Requirement of Drosophila NF1 for activation of adenylyl cyclase by PACAP38-like neuropeptides (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: The human neurofibromatosis type 1 (NF1) tumor suppressor protein functions as a Ras-specific guanosine triphosphatase-activating protein, but the identity of Ras- mediated pathways modulated by NF1 remains unknown. A study of Drosophila NF1 mutants revealed that NF1 is essential for the cellular response to the neuropeptide PACAP38 (pituitary adenylyl cyclase-activating polypeptide) at the neuromuscular junction. The peptide induced a 100-fold enhancement of potassium currents by activating the Ras-Raf and adenylyl cyclase-adenosine 3',5'-monophosphate (cAMP) pathways. This response was eliminated in NF1 mutants. NF1 appears to regulate the rutabaga-encoded adenylyl cyclase rather than the Ras-Raf pathway. Moreover, the NF1 defect was rescued by the exposure of cells to pharmacological treatment that increased concentrations of cAMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, H F -- The, I -- Hannan, F -- Bernards, A -- Zhong, Y -- R01-NS31747/NS/NINDS NIH HHS/ -- R01-NS34779/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 May 2;276(5313):795-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115204" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Adenylyl Cyclases/*metabolism ; Animals ; Animals, Genetically Modified ; Bucladesine/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Drosophila/*enzymology/genetics ; *Drosophila Proteins ; Enzyme Activation ; Genes, Insect ; In Vitro Techniques ; Insect Proteins/genetics/*physiology ; Mutation ; *Nerve Tissue Proteins ; Neuromuscular Junction/drug effects/*enzymology ; Neuropeptides/metabolism/*pharmacology ; Patch-Clamp Techniques ; Pituitary Adenylate Cyclase-Activating Polypeptide ; Potassium/metabolism ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I ; Receptors, Pituitary Hormone/metabolism ; Signal Transduction ; *ras GTPase-Activating Proteins ; ras Proteins/metabolism
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    Pericyte loss and microaneurysm formation in PDGF-B-deficient mice (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindahl, P -- Johansson, B R -- Leveen, P -- Betsholtz, C -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, University of Goteborg, Medicinaregatan 9A, S-413 90 Goteborg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211853" target="_blank"〉PubMed〈/a〉
    Keywords: Aneurysm/*etiology ; Animals ; Brain/blood supply ; Capillaries/*cytology/embryology/metabolism ; Cell Movement ; Endothelium, Vascular/cytology/metabolism ; Hemorrhage/etiology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neovascularization, Physiologic ; Platelet-Derived Growth Factor/deficiency/genetics/*physiology ; Proto-Oncogene Proteins/deficiency/genetics/*physiology ; Proto-Oncogene Proteins c-sis ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Platelet-Derived Growth Factor beta ; Receptor, TIE-2 ; Receptors, Platelet-Derived Growth Factor/metabolism ; Signal Transduction ; Stem Cells/cytology/metabolism ; Up-Regulation
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    Activation of heat shock transcription factor 3 by c-Myb in the absence of cellular stress (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: In vertebrates, the presence of multiple heat shock transcription factors (HSFs) indicates that these factors may be regulated by distinct stress signals. HSF3 was specifically activated in unstressed proliferating cells by direct binding to the c-myb proto-oncogene product (c-Myb). These factors formed a complex through their DNA binding domains that stimulated the nuclear entry and formation of the transcriptionally active trimer of HSF3. Because c-Myb participates in cellular proliferation, this regulatory pathway may provide a link between cellular proliferation and the stress response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanei-Ishii, C -- Tanikawa, J -- Nakai, A -- Morimoto, R I -- Ishii, S -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):246-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Tsukuba Life Science Center, RIKEN, Tsukuba, Ibaraki 305, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle ; Cell Line ; Cell Nucleus/metabolism ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-myb ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/*metabolism ; Transcriptional Activation ; Transfection
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    The Ras-RasGAP complex: structural basis for GTPase activation and its loss in oncogenic Ras mutants (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-07-18
    Description: The three-dimensional structure of the complex between human H-Ras bound to guanosine diphosphate and the guanosine triphosphatase (GTPase)-activating domain of the human GTPase-activating protein p120GAP (GAP-334) in the presence of aluminum fluoride was solved at a resolution of 2.5 angstroms. The structure shows the partly hydrophilic and partly hydrophobic nature of the communication between the two molecules, which explains the sensitivity of the interaction toward both salts and lipids. An arginine side chain (arginine-789) of GAP-334 is supplied into the active site of Ras to neutralize developing charges in the transition state. The switch II region of Ras is stabilized by GAP-334, thus allowing glutamine-61 of Ras, mutation of which activates the oncogenic potential, to participate in catalysis. The structural arrangement in the active site is consistent with a mostly associative mechanism of phosphoryl transfer and provides an explanation for the activation of Ras by glycine-12 and glutamine-61 mutations. Glycine-12 in the transition state mimic is within van der Waals distance of both arginine-789 of GAP-334 and glutamine-61 of Ras, and even its mutation to alanine would disturb the arrangements of residues in the transition state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheffzek, K -- Ahmadian, M R -- Kabsch, W -- Wiesmuller, L -- Lautwein, A -- Schmitz, F -- Wittinghofer, A -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):333-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur molekulare Physiologie, Abteilung Strukturelle Biologie, Rheinlanddamm 201, 44139 Dortmund, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219684" target="_blank"〉PubMed〈/a〉
    Keywords: Aluminum Compounds/chemistry/metabolism ; Amino Acid Sequence ; Binding Sites ; Catalysis ; Cell Transformation, Neoplastic ; Crystallography, X-Ray ; Enzyme Activation ; Fluorides/chemistry/metabolism ; GTP Phosphohydrolases/chemistry/*metabolism ; GTP-Binding Proteins/chemistry/metabolism ; GTPase-Activating Proteins ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Models, Molecular ; Molecular Sequence Data ; Mutation ; *Protein Conformation ; Protein Structure, Secondary ; Proteins/*chemistry/*metabolism ; Signal Transduction ; ras GTPase-Activating Proteins ; ras Proteins/chemistry/genetics/*metabolism
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    PAS, present, and future: clues to the origins of circadian clocks (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kay, S A -- New York, N.Y. -- Science. 1997 May 2;276(5313):753-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Science Foundation Center for Biological Timing, Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. stevek@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Clocks ; *Circadian Rhythm ; DNA-Binding Proteins/chemistry/genetics/*physiology ; Drosophila/genetics/physiology ; Drosophila Proteins ; Fungal Proteins/genetics/physiology ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Light ; Neurospora/chemistry/genetics/*physiology ; Nuclear Proteins/chemistry/genetics/physiology ; Period Circadian Proteins ; Signal Transduction ; Transcription Factors/chemistry/genetics/*physiology
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    A di-acidic signal required for selective export from the endoplasmic reticulum (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-07-25
    Description: Transport of membrane proteins between intracellular compartments requires specific sequences in the protein cytoplasmic domain to direct packaging into vesicle shuttles. A sequence that mediates export from the endoplasmic reticulum (ER) has proved elusive. A di-acidic signal (Asp-X-Glu, where X represents any amino acid) on the cytoplasmic tail of vesicular stomatitis virus glycoprotein (VSV-G) and other cargo molecules was required for efficient recruitment to vesicles mediating export from the ER in baby hamster kidney cells. The existence of such a signal provides evidence that export from the ER occurs through a selective mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishimura, N -- Balch, W E -- GM 42336/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):556-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228004" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Phosphatase/metabolism ; Amino Acid Sequence ; Animals ; Biological Transport ; Cell Line ; Cricetinae ; Cytoplasm/chemistry ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; *Membrane Glycoproteins ; Membrane Proteins/*chemistry/*metabolism ; Molecular Sequence Data ; Mutation ; Protein Folding ; Protein Sorting Signals/chemistry/*metabolism ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Viral Envelope Proteins/*chemistry/*metabolism
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    Human cancer syndromes: clues to the origin and nature of cancer (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-11-14
    Description: More than 20 different hereditary cancer syndromes have now been defined and attributed to specific germline mutations in various inherited cancer genes. Collectively, the syndromes affect about 1 percent of cancer patients. An individual who carries a mutant allele of an inherited cancer gene has a variable risk of cancer that is influenced by the particular mutation, other cellular genes, and dietary, lifestyle, and environmental factors. Though hereditary cancer syndromes are rare, their study has provided powerful insights into more common forms of cancer. Somatic mutations in sporadic cancers frequently alter the inherited cancer genes, and the functions of cell signaling pathways have been illuminated by study of the affected genes. Further investigation of inherited mutations that affect susceptibility to cancer will aid efforts to effectively prevent, detect, and treat the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fearon, E R -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1043-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Michigan Medical Center, 4301 MSRB III, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0638, USA. efearon@mmg.im.med.umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353177" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Disease Models, Animal ; *Genes, Tumor Suppressor ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genetic Variation ; Humans ; *Mutation ; Neoplastic Syndromes, Hereditary/*genetics ; *Oncogenes ; Organ Specificity ; Penetrance ; Signal Transduction
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    Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-08-08
    Description: TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheridan, J P -- Marsters, S A -- Pitti, R M -- Gurney, A -- Skubatch, M -- Baldwin, D -- Ramakrishnan, L -- Gray, C L -- Baker, K -- Wood, W I -- Goddard, A D -- Godowski, P -- Ashkenazi, A -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, South San Francisco, CA 94080-4918, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242611" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; GPI-Linked Proteins ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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    daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-08-15
    Description: A C. elegans neurosecretory signaling system regulates whether animals enter the reproductive life cycle or arrest development at the long-lived dauer diapause stage. daf-2, a key gene in the genetic pathway that mediates this endocrine signaling, encodes an insulin receptor family member. Decreases in DAF-2 signaling induce metabolic and developmental changes, as in mammalian metabolic control by the insulin receptor. Decreased DAF-2 signaling also causes an increase in life-span. Life-span regulation by insulin-like metabolic control is analogous to mammalian longevity enhancement induced by caloric restriction, suggesting a general link between metabolism, diapause, and longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, K D -- Tissenbaum, H A -- Liu, Y -- Ruvkun, G -- R01AG14161/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):942-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252323" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/chemistry/*genetics/growth & development/metabolism ; Caenorhabditis elegans Proteins ; Chromosome Mapping ; Conserved Sequence ; Energy Intake ; *Genes, Helminth ; Glucose/metabolism ; Humans ; Insulin/metabolism ; Larva/genetics/growth & development/metabolism ; Longevity/*genetics ; Molecular Sequence Data ; Mutation ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Receptor, IGF Type 1/chemistry/genetics ; Receptor, Insulin/chemistry/*genetics/metabolism ; Signal Transduction
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    Primary target (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1997 Sep 19;277(5333):1848.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9324771" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Clone Cells ; Culture Media ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/*genetics ; Gene Deletion ; Gene Targeting/*methods ; Genetic Vectors ; Humans
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  • 34
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    Xenotransplanters turn xenovirologists (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1893.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Coculture Techniques ; Gammaretrovirus/genetics/*physiology ; Genome, Viral ; Humans ; Retroviridae Infections/transmission ; Swine/genetics/*virology ; *Transplantation, Heterologous
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    Cellular differentiation regulated by gibberellin in the Arabidopsis thaliana pickle mutant (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-07-04
    Description: The plant growth regulator gibberellin (GA) has a profound effect on shoot development and promotes developmental transitions such as flowering. Little is known about any analogous effect GA might have on root development. In a screen for mutants, Arabidopsis plants carrying a mutation designated pickle (pkl) were isolated in which the primary root meristem retained characteristics of embryonic tissue. Expression of this aberrant differentiation state was suppressed by GA. Root tissue from plants carrying the pkl mutation spontaneously regenerated new embryos and plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogas, J -- Cheng, J C -- Sung, Z R -- Somerville, C -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):91-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution of Washington, 290 Panama Street, Stanford, CA 94305, USA. jogas@andrew.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204906" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*cytology/drug effects/genetics/metabolism ; *Arabidopsis Proteins ; Cell Differentiation/drug effects ; Fatty Acids/analysis ; Genes, Plant ; Germination ; Gibberellins/*metabolism/pharmacology ; Meristem/*cytology/drug effects/metabolism ; Mutation ; Phenotype ; Plant Growth Regulators/pharmacology ; Plant Proteins/genetics ; Plant Roots/*cytology/drug effects/metabolism ; Signal Transduction ; Triazoles/pharmacology ; Triglycerides/analysis
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    Cdc25 mitotic inducer targeted by chk1 DNA damage checkpoint kinase (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-09-05
    Description: Arrest of the cell cycle at the G2 checkpoint, induced by DNA damage, requires inhibitory phosphorylation of the kinase Cdc2 in both fission yeast and human cells. The kinase Wee1 and the phosphatase Cdc25, which regulate Cdc2 phosphorylation, were evaluated as targets of Chk1, a kinase essential for the checkpoint. Fission yeast cdc2-3w Deltacdc25 cells, which express activated Cdc2 and lack Cdc25, were responsive to Wee1 but insensitive to Chk1 and irradiation. Expression of large amounts of Chk1 produced the same phenotype as did loss of the cdc25 gene in cdc2-3w cells. Cdc25 associated with Chk1 in vivo and was phosphorylated when copurified in Chk1 complexes. These findings identify Cdc25, but not Wee1, as a target of the DNA damage checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Furnari, B -- Rhind, N -- Russell, P -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1495-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278510" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; CDC2 Protein Kinase/*metabolism ; Cell Cycle Proteins/*metabolism ; Cell Division ; *DNA Damage ; DNA Helicases/metabolism ; Fungal Proteins/*metabolism ; G2 Phase ; Gamma Rays ; Genes, Fungal ; *Mitosis ; Models, Biological ; Mutation ; *Nuclear Proteins ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae Proteins ; Schizosaccharomyces/cytology/genetics/*metabolism/radiation effects ; Schizosaccharomyces pombe Proteins ; Signal Transduction ; Temperature ; *ras-GRF1
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    The product of the proto-oncogene c-cbl: a negative regulator of the Syk tyrosine kinase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: Engagement of antigen and immunoglobulin receptors on hematopoietic cells is directly coupled to activation of nonreceptor protein tyrosine kinases (PTKs) that then phosphorylate critical intracellular substrates. In mast cells stimulated through the FcvarepsilonRI receptor, activation of several PTKs including Syk leads to degranulation and release of such mediators of the allergic response as histamine and serotonin. Regulation of Syk function occurred through interaction with the Cbl protein, itself a PTK substrate in this system. Overexpression of Cbl led to inhibition of Syk and suppression of serotonin release from mast cells, demonstrating its ability to inhibit a nonreceptor tyrosine kinase. Complex adaptor proteins such as Cbl can directly regulate the functions of the proteins they bind.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ota, Y -- Samelson, L E -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-5430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Degranulation ; Enzyme Precursors/antagonists & inhibitors/*metabolism ; Genetic Vectors ; Intracellular Signaling Peptides and Proteins ; Mast Cells/*metabolism ; Mutation ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Rats ; Receptors, IgE/metabolism ; Receptors, IgG/metabolism ; Recombinant Proteins/metabolism ; Serotonin/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; *Ubiquitin-Protein Ligases ; Vaccinia virus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Independent and additive effects of central POMC and leptin pathways on murine obesity (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: The lethal yellow (AY/a) mouse has a defect in proopiomelanocortin (POMC) signaling in the brain that leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin. It has been proposed that the weight-reducing effects of leptin are thus transmitted primarily by way of POMC neurons. However, the central effects of defective POMC signaling, and the absence of leptin, on weight gain in double-mutant lethal yellow (AY/a) leptin-deficient (lepob/lepob) mice were shown to be independent and additive. Furthermore, deletion of the leptin gene restored leptin sensitivity to AY/a mice. This result implies that in the AY/a mouse, obesity is independent of leptin action, and resistance to leptin results from desensitization of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boston, B A -- Blaydon, K M -- Varnerin, J -- Cone, R D -- DK/AR517330/DK/NIDDK NIH HHS/ -- DK02404/DK/NIDDK NIH HHS/ -- HD33703/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Oregon Health Sciences University, Portland, OR 97201, USA. Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374468" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Agouti Signaling Protein ; Alleles ; Animals ; Arcuate Nucleus of Hypothalamus/*metabolism ; Blood Glucose/analysis ; Corticosterone/blood ; Crosses, Genetic ; Eating/drug effects ; Energy Metabolism ; Female ; Homeostasis ; Insulin/blood ; *Intercellular Signaling Peptides and Proteins ; Leptin ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Neurons/metabolism ; Obesity/genetics/*metabolism ; Pro-Opiomelanocortin/*metabolism ; Proteins/genetics/*metabolism/pharmacology ; Signal Transduction ; Weight Gain
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 39
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    SV40 and human cancer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayflick, L -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):337-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Haplorhini ; Humans ; Poliovirus/growth & development ; *Poliovirus Vaccine, Inactivated ; Simian virus 40/*pathogenicity ; United States ; United States Food and Drug Administration ; Virus Cultivation
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  • 40
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    A member of the Frizzled protein family mediating axis induction by Wnt-5A (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: In Xenopus laevis embryos, the Wingless/Wnt-1 subclass of Wnt molecules induces axis duplication, whereas the Wnt-5A subclass does not. This difference could be explained by distinct signal transduction pathways or by a lack of one or more Wnt-5A receptors during axis formation. Wnt-5A induced axis duplication and an ectopic Spemann organizer in the presence of hFz5, a member of the Frizzled family of seven-transmembrane receptors. Wnt-5A/hFz5 signaling was antagonized by glycogen synthase kinase-3 and by the amino-terminal ectodomain of hFz5. These results identify hFz5 as a receptor for Wnt-5A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, X -- Saint-Jeannet, J P -- Wang, Y -- Nathans, J -- Dawid, I -- Varmus, H -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1652-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, Building 49, Room 4A56, National Institutes of Health, Bethesda, MD 20892, USA. xhe.nhgri.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; DNA-Binding Proteins/genetics ; *Drosophila Proteins ; *Embryonic Development ; *Embryonic Induction ; Frizzled Receptors ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Goosecoid Protein ; *Homeodomain Proteins ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Proteins/genetics/*metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, G-Protein-Coupled ; *Repressor Proteins ; Signal Transduction ; *Transcription Factors ; Wnt Proteins ; *Xenopus Proteins ; Xenopus laevis/embryology
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  • 41
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    A mammalian telomerase-associated protein (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: The telomerase ribonucleoprotein catalyzes the addition of new telomeres onto chromosome ends. A gene encoding a mammalian telomerase homolog called TP1 (telomerase-associated protein 1) was identified and cloned. TP1 exhibited extensive amino acid similarity to the Tetrahymena telomerase protein p80 and was shown to interact specifically with mammalian telomerase RNA. Antiserum to TP1 immunoprecipitated telomerase activity from cell extracts, suggesting that TP1 is associated with telomerase in vivo. The identification of TP1 suggests that telomerase-associated proteins are conserved from ciliates to humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrington, L -- McPhail, T -- Mar, V -- Zhou, W -- Oulton, R -- Bass, M B -- Arruda, I -- Robinson, M O -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):973-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arruda, Ontario Cancer Institute-Amgen Institute, Department of Medical Biophysics, University of Toronto, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020079" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Carrier Proteins/*chemistry/genetics/immunology/*metabolism ; Cell Line ; Cloning, Molecular ; DNA, Complementary/genetics ; Humans ; Mice ; Molecular Sequence Data ; Precipitin Tests ; RNA/*metabolism ; RNA, Messenger/genetics/metabolism ; Sequence Homology, Amino Acid ; Telomerase/*chemistry/genetics/metabolism ; Tetrahymena/chemistry/genetics ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
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    NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Activation of the nuclear factor of activated T cells transcription factor (NF-AT) is a key event underlying lymphocyte action. The CAML (calcium-modulator and cyclophilin ligand) protein is a coinducer of NF-AT activation when overexpressed in Jurkat T cells. A member of the tumor necrosis factor receptor superfamily was isolated by virtue of its affinity for CAML. Cross-linking of this lymphocyte-specific protein, designated TACI (transmembrane activator and CAML-interactor), on the surface of transfected Jurkat cells with TACI-specific antibodies led to activation of the transcription factors NF-AT, AP-1, and NFkappaB. TACI-induced activation of NF-AT was specifically blocked by a dominant-negative CAML mutant, thus implicating CAML as a signaling intermediate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bulow, G U -- Bram, R J -- CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):138-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Oncology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311921" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Calcineurin ; Calmodulin-Binding Proteins/metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Jurkat Cells ; Lymphocyte Activation ; *Membrane Proteins ; Molecular Sequence Data ; Mutation ; NF-kappa B/metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoprotein Phosphatases/metabolism ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Sequence Alignment ; Signal Transduction ; T-Lymphocytes/immunology/*metabolism ; Transcription Factor AP-1/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic ; Transfection ; Transmembrane Activator and CAML Interactor Protein
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    Requirement for GD3 ganglioside in CD95- and ceramide-induced apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Gangliosides participate in development and tissue differentiation. Cross-linking of the apoptosis-inducing CD95 protein (also called Fas or APO-1) in lymphoid and myeloid tumor cells triggered GD3 ganglioside synthesis and transient accumulation. CD95-induced GD3 accumulation depended on integral receptor "death domains" and on activation of a family of cysteine proteases called caspases. Cell-permeating ceramides, which are potent inducers of apoptosis, also triggered GD3 synthesis. GD3 disrupted mitochondrial transmembrane potential (DeltaPsim), and induced apoptosis, in a caspase-independent fashion. Transient overexpression of the GD3 synthase gene directly triggered apoptosis. Pharmacological inhibition of GD3 synthesis and exposure to GD3 synthase antisense oligodeoxynucleotides prevented CD95-induced apoptosis. Thus, GD3 ganglioside mediates the propagation of CD95-generated apoptotic signals in hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Maria, R -- Lenti, L -- Malisan, F -- d'Agostino, F -- Tomassini, B -- Zeuner, A -- Rippo, M R -- Testi, R -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1652-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Medicine and Biochemical Sciences, University of Rome "Tor Vergata," 00133 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287216" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD95/metabolism/*physiology ; *Apoptosis ; Ceramides/pharmacology/*physiology ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Gangliosides/biosynthesis/*metabolism/pharmacology ; Golgi Apparatus/metabolism ; Humans ; Membrane Potentials ; Mitochondria/physiology ; Morpholines/pharmacology ; Oligonucleotides, Antisense/pharmacology ; Sialyltransferases/genetics/metabolism ; Signal Transduction ; Transfection ; Tumor Cells, Cultured
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  • 44
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    CD4-independent binding of SIV gp120 to rhesus CCR5 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: CCR5 and CD4 are coreceptors for immunodeficiency virus entry into target cells. The gp120 envelope glycoprotein from human immunodeficiency virus strain HIV-1(YU2) bound human CCR5 (CCR5hu) or rhesus macaque CCR5 (CCR5rh) only in the presence of CD4. The gp120 from simian immunodeficiency virus strain SIVmac239 bound CCR5rh without CD4, but CCR5hu remained CD4-dependent. The CD4-independent binding of SIVmac239 gp120 depended on a single amino acid, Asp13, in the CCR5rh amino-terminus. Thus, CCR5-binding moieties on the immunodeficiency virus envelope glycoprotein can be generated by interaction with CD4 or by direct interaction with the CCR5 amino-terminus. These results may have implications for the evolution of receptor use among lentiviruses as well as utility in the development of effective intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, K A -- Wyatt, R -- Farzan, M -- Choe, H -- Marcon, L -- Desjardins, E -- Robinson, J -- Sodroski, J -- Gerard, C -- Gerard, N P -- AI41581/AI/NIAID NIH HHS/ -- HL36162/HL/NHLBI NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1470-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perlmutter Laboratory, Children's Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9367961" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Antigens, CD4/*physiology ; Cell Line ; HIV Antibodies/immunology ; HIV Envelope Protein gp120/chemistry/*metabolism ; HIV-2/immunology ; Humans ; Macaca mulatta ; Macrophages/virology ; *Membrane Glycoproteins ; Mutation ; Receptors, CCR5/chemistry/*metabolism ; Simian Immunodeficiency Virus/*metabolism ; Transfection ; *Viral Envelope Proteins
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  • 45
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    Inhibition of brain Gz GAP and other RGS proteins by palmitoylation of G protein alpha subunits (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-14
    Description: Palmitoylation of the alpha subunit of the guanine nucleotide-binding protein Gz inhibited by more than 90 percent its response to the guanosine triphosphatase (GTPase)-accelerating activity of Gz GAP, a Gz-selective member of the regulators of G-protein signaling (RGS) protein family of GTPase-activating proteins (GAPs). Palmitoylation both decreased the affinity of Gz GAP for the GTP-bound form of Galphaz by at least 90 percent and decreased the maximum rate of GTP hydrolysis. Inhibition was reversed by removal of the palmitoyl group by dithiothreitol. Palmitoylation of Galphaz also inhibited its response to the GAP activity of Galpha-interacting protein (GAIP), another RGS protein, and palmitoylation of Galphai1 inhibited its response to RGS4. The extent of inhibition of Gz GAP, GAIP, RGS4, and RGS10 correlated roughly with their intrinsic GAP activities for the Galpha target used in the assay. Reversible palmitoylation is thus a major determinant of Gz deactivation after its stimulation by receptors, and may be a general mechanism for prolonging or potentiating G-protein signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tu, Y -- Wang, J -- Ross, E M -- GM30355/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1132-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9041, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353196" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Dithiothreitol/pharmacology ; *GTP-Binding Protein alpha Subunits ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Guanosine Triphosphate/metabolism ; *Heterotrimeric GTP-Binding Proteins ; Hydrolysis ; Kinetics ; Palmitic Acid/*metabolism ; Palmitoyl Coenzyme A/metabolism ; Phosphoproteins/antagonists & inhibitors/metabolism ; Proteins/*antagonists & inhibitors/metabolism ; *RGS Proteins ; Signal Transduction
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    Worm longevity gene cloned (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):897-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9281069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/growth & development/metabolism ; Caenorhabditis elegans Proteins ; Cloning, Molecular ; Energy Intake ; *Genes, Helminth ; Glucose/metabolism ; Humans ; Insulin/metabolism ; Longevity/*genetics ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/genetics/metabolism ; Receptor, Insulin/*genetics/metabolism ; Second Messenger Systems ; Signal Transduction
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  • 47
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    Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-24
    Description: BAD is a distant member of the Bcl-2 family that promotes cell death. Phosphorylation of BAD prevents this. BAD phosphorylation induced by interleukin-3 (IL-3) was inhibited by specific inhibitors of phosphoinositide 3-kinase (PI 3-kinase). Akt, a survival-promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase-dependent manner. Active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3. Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉del Peso, L -- Gonzalez-Garcia, M -- Page, C -- Herrera, R -- Nunez, G -- CA-64556/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381178" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; Apoptosis ; Carrier Proteins/*metabolism ; Cell Line ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Humans ; Interleukin-3/*pharmacology ; Mice ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; bcl-Associated Death Protein ; bcl-X Protein
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  • 48
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    Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by beta-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of beta-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of beta-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta-catenin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morin, P J -- Sparks, A B -- Korinek, V -- Barker, N -- Clevers, H -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1787-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065402" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Germ-Line Mutation ; Humans ; Mutation ; Phosphorylation ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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  • 49
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    Targeting of HIV- and SIV-infected cells by CD4-chemokine receptor pseudotypes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Retroviral vectors containing CD4 and an appropriate chemokine receptor were evaluated for the ability to transduce cells infected with human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). These CD4-chemokine receptor pseudotypes were able to target HIV- and SIV-infected cell lines and monocyte-derived macrophages in a manner that corresponded to the specificity of the viral envelope glycoprotein for its CD4-chemokine receptor complex. This approach could offer a way to deliver antiviral genes directly to HIV-infected cells in vivo and could provide an additional treatment strategy in conjunction with existing antiviral therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Endres, M J -- Jaffer, S -- Haggarty, B -- Turner, J D -- Doranz, B J -- O'Brien, P J -- Kolson, D L -- Hoxie, J A -- AI33854/AI/NIAID NIH HHS/ -- AI40880/AI/NIAID NIH HHS/ -- HL 07439/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Hematology-Oncology Division, University of Pennsylvania, Philadelphia, PA 19104, USA. endres@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9367958" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*genetics/metabolism ; Cell Line ; Gene Products, env/metabolism ; *Gene Transfer Techniques ; *Genetic Vectors ; HIV-1/*physiology ; Humans ; Macrophages/virology ; Plasmids ; Receptors, CCR5/genetics/metabolism ; Receptors, CXCR4/genetics/metabolism ; Receptors, Chemokine/*genetics/metabolism ; Simian Immunodeficiency Virus/*physiology ; Transfection
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    Calcium waves in retinal glial cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-07
    Description: Calcium signals were recorded from glial cells in acutely isolated rat retina to determine whether Ca2+ waves occur in glial cells of intact central nervous system tissue. Chemical (adenosine triphosphate), electrical, and mechanical stimulation of astrocytes initiated increases in the intracellular concentration of Ca2+ that propagated at approximately 23 micrometers per second through astrocytes and Muller cells as intercellular waves. The Ca2+ waves persisted in the absence of extracellular Ca2+ but were largely abolished by thapsigargin and intracellular heparin, indicating that Ca2+ was released from intracellular stores. The waves did not evoke changes in cell membrane potential but traveled synchronously in astrocytes and Muller cells, suggesting a functional linkage between these two types of glial cells. Such glial Ca2+ waves may constitute an extraneuronal signaling pathway in the central nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410141/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410141/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, E A -- Zahs, K R -- EY04077/EY/NEI NIH HHS/ -- EY10383/EY/NEI NIH HHS/ -- R01 EY004077/EY/NEI NIH HHS/ -- R01 EY004077-19/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):844-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Minnesota, 435 Delaware Street, SE, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9012354" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Astrocytes/*metabolism ; Calcium/*metabolism ; Calcium Channels/metabolism ; Electric Stimulation ; Heparin/pharmacology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate Receptors ; Kinetics ; Membrane Potentials ; Neuroglia/*metabolism ; Physical Stimulation ; Rats ; Receptors, Cytoplasmic and Nuclear/metabolism ; Retina/*cytology/metabolism ; Signal Transduction ; Stimulation, Chemical ; Thapsigargin/pharmacology
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    Nuclear export of NF-ATc enhanced by glycogen synthase kinase-3 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: The transcription factor NF-AT responds to Ca2+-calcineurin signals by translocating to the nucleus, where it participates in the activation of early immune response genes. Calcineurin dephosphorylates conserved serine residues in the amino terminus of NF-AT, resulting in nuclear import. Purification of the NF-AT kinase revealed that it is composed of a priming kinase activity and glycogen synthase kinase-3 (GSK-3). GSK-3 phosphorylates conserved serines necessary for nuclear export, promotes nuclear exit, and thereby opposes Ca2+-calcineurin signaling. Because GSK-3 responds to signals initiated by Wnt and other ligands, NF-AT family members could be effectors of these pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beals, C R -- Sheridan, C M -- Turck, C W -- Gardner, P -- Crabtree, G R -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1930-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072970" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Brain/enzymology ; COS Cells ; Calcineurin ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Calmodulin-Binding Proteins/metabolism ; Cell Nucleus/*metabolism ; Cloning, Molecular ; Cyclic AMP-Dependent Protein Kinases/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; Transfection
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    Activation of SAPK/JNK by TNF receptor 1 through a noncytotoxic TRAF2-dependent pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: Interaction of the p55 tumor necrosis factor receptor 1 (TNF-R1)-associated signal transducer TRADD with FADD signals apoptosis, whereas the TNF receptor-associated factor 2 protein (TRAF2) is required for activation of the nuclear transcription factor nuclear factor kappa B. TNF-induced activation of the stress-activated protein kinase (SAPK) was shown to occur through a noncytotoxic TRAF2-dependent pathway. TRAF2 was both sufficient and necessary for activation of SAPK by TNF-R1; conversely, expression of a dominant-negative FADD mutant, which blocks apoptosis, did not interfere with SAPK activation. Therefore, SAPK activation occurs through a pathway that is not required for TNF-R1-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natoli, G -- Costanzo, A -- Ianni, A -- Templeton, D J -- Woodgett, J R -- Balsano, C -- Levrero, M -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):200-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fondazione Andrea Cesalpino and Istituto di I Clinica Medica, Policlinico Umberto I, Viale del Policlinico 155, 00161 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985011" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/pharmacology ; *Adaptor Proteins, Signal Transducing ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; Cell Line ; Dactinomycin/pharmacology ; Enzyme Activation ; Fas-Associated Death Domain Protein ; Free Radical Scavengers/pharmacology ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *MAP Kinase Kinase Kinase 1 ; *Mitogen-Activated Protein Kinases ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/*metabolism ; Reactive Oxygen Species/metabolism ; Receptors, Tumor Necrosis Factor/*metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A cyanobacterial phytochrome two-component light sensory system (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: The biliprotein phytochrome regulates plant growth and developmental responses to the ambient light environment through an unknown mechanism. Biochemical analyses demonstrate that phytochrome is an ancient molecule that evolved from a more compact light sensor in cyanobacteria. The cyanobacterial phytochrome Cph1 is a light-regulated histidine kinase that mediates red, far-red reversible phosphorylation of a small response regulator, Rcp1 (response regulator for cyanobacterial phytochrome), encoded by the adjacent gene, thus implicating protein phosphorylation-dephosphorylation in the initial step of light signal transduction by phytochrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, K C -- Wu, S H -- Murphy, J T -- Lagarias, J C -- 1 P41 RR06009/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1505-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular and Cellular Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278513" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Bacterial Proteins ; Cloning, Molecular ; Cyanobacteria/chemistry/genetics/*metabolism ; Genes, Bacterial ; *Light ; Molecular Sequence Data ; Operon ; Phosphorylation ; Protein Kinases/chemistry/genetics/*metabolism ; Proteins ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Deletion ; Signal Transduction
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    Selective expression of the eotaxin receptor CCR3 by human T helper 2 cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: There is growing evidence that T helper cell subsets (TH1 and TH2) can be differentially recruited to promote different types of inflammatory reactions. Murine TH1 but not TH2 cells are recruited through P- and E-selectin into inflamed tissues, where they induce delayed-type hypersensitivity reactions. The human eotaxin-receptor CCR3, originally described on eosinophils and basophils, was also found to be expressed by TH2 cells. An antibody to CCR3 was used to isolate T cells from peripheral blood that give rise to TH2-polarized cell lines and to identify TH2 cells derived from naive T cells in vitro. Eotaxin stimulated increases in intracellular calcium and chemotaxis of CCR3(+) T cells. The attraction of TH2 cells by eotaxin could represent a key mechanism in allergic reactions, because it promotes the allergen-driven production of interleukin-4 and interleukin-5 necessary to activate basophils and eosinophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sallusto, F -- Mackay, C R -- Lanzavecchia, A -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2005-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Grenzacherstrasse 487, CH-4005 Basel, Switzerland. sallusto@bii.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302298" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Calcium/metabolism ; Cell Line ; Cell Separation ; Chemokine CCL11 ; *Chemokines, CC ; Chemotaxis, Leukocyte ; Clone Cells ; Cytokines/metabolism/*pharmacology ; Humans ; Interferon-alpha/pharmacology ; Interferon-gamma/biosynthesis ; Interleukin-3/biosynthesis ; Interleukin-4/biosynthesis ; Receptors, CCR3 ; *Receptors, Chemokine ; Receptors, Cytokine/*metabolism ; Th2 Cells/*metabolism/*physiology ; Transforming Growth Factor beta/pharmacology
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    An animal model for acute and persistent Epstein-Barr virus infection (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: Epstein-Barr virus (EBV) is a human lymphocryptovirus that causes infectious mononucleosis, persists asymptomatically for life in nearly all adults, and is associated with the development of B cell lymphomas and nasopharyngeal carcinomas. A highly similar rhesus lymphocryptovirus naturally endemic in rhesus monkeys was used to orally infect naive animals from a pathogen-free colony. This animal model reproduced key aspects of human EBV infection, including oral transmission, atypical lymphocytosis, lymphadenopathy, activation of CD23(+) peripheral blood B cells, sustained serologic responses to lytic and latent EBV antigens, latent infection in the peripheral blood, and virus persistence in oropharyngeal secretions. This system may be useful for studying the pathogenesis, prevention, and treatment of EBV infection and associated oncogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moghaddam, A -- Rosenzweig, M -- Lee-Parritz, D -- Annis, B -- Johnson, R P -- Wang, F -- CA65319/CA/NCI NIH HHS/ -- CA68051/CA/NCI NIH HHS/ -- P51RR00168/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2030-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197263" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/blood ; B-Lymphocytes/immunology/virology ; Cell Line ; DNA, Viral/analysis ; *Disease Models, Animal ; *Herpesviridae Infections/immunology/pathology/virology ; *Herpesvirus 4, Human ; Humans ; Immunoenzyme Techniques ; *Lymphocryptovirus/immunology/isolation & purification ; Lymphocyte Activation ; *Macaca mulatta ; Mouth/virology ; Oropharynx/virology ; Receptors, IgE/blood ; Specific Pathogen-Free Organisms ; *Tumor Virus Infections/immunology/pathology/virology ; Virus Latency ; Virus Shedding
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    Regulation of distinct stages of skeletal muscle differentiation by mitogen-activated protein kinases (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: The signal transduction pathway or pathways linking extracellular signals to myogenesis are poorly defined. Upon mitogen withdrawal from C2C12 myoblasts, the mitogen-activated protein kinase (MAPK) p42Erk2 is inactivated concomitant with up-regulation of muscle-specific genes. Overexpression of MAPK phosphatase-1 (MKP-1) inhibited p42Erk2 activity and was sufficient to relieve the inhibitory effects of mitogens on muscle-specific gene expression. Later during myogenesis, endogenous expression of MKP-1 decreased. MKP-1 overexpression during differentiation prevented myotube formation despite appropriate expression of myosin heavy chain. This indicates that muscle-specific gene expression is necessary but not sufficient to commit differentiated myocytes to myotubes and suggests a function for the MAPKs during the early and late stages of skeletal muscle differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bennett, A M -- Tonks, N K -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Demerec Building, 1 Bungtown Road, Post Office Box 100, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; *Cell Cycle Proteins ; Cell Differentiation ; Cell Division ; Cell Line ; Cloning, Molecular ; Culture Media ; Cyclin D1/genetics ; Dual Specificity Phosphatase 1 ; Gene Expression Regulation, Developmental ; Immediate-Early Proteins/genetics/*metabolism ; JNK Mitogen-Activated Protein Kinases ; Mice ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors/*metabolism ; *Mitogen-Activated Protein Kinases ; Mitogens/pharmacology ; Muscle Proteins/*genetics ; Muscle, Skeletal/*cytology/*enzymology/metabolism ; *Phosphoprotein Phosphatases ; Phosphorylation ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Tetracycline/pharmacology ; Transcription, Genetic
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    Quenching the spark in the heart (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yue, D T -- New York, N.Y. -- Science. 1997 May 2;276(5313):755-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Program in Molecular and Cellular Systems Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dyue@bme.jhu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157553" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium Channels, L-Type ; Cardiomegaly/*physiopathology ; Heart Failure/*physiopathology ; Humans ; Microscopy, Confocal ; Muscle Proteins/metabolism ; Myocardial Contraction/*physiology ; Myocardium/*metabolism ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum/metabolism ; Signal Transduction
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    Structure of the carboxyl-terminal dimerization domain of the HIV-1 capsid protein (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-05
    Description: The carboxyl-terminal domain, residues 146 to 231, of the human immunodeficiency virus-1 (HIV-1) capsid protein [CA(146-231)] is required for capsid dimerization and viral assembly. This domain contains a stretch of 20 residues, called the major homology region (MHR), which is conserved across retroviruses and is essential for viral assembly, maturation, and infectivity. The crystal structures of CA(146-231) and CA(151-231) reveal that the globular domain is composed of four helices and an extended amino-terminal strand. CA(146-231) dimerizes through parallel packing of helix 2 across a dyad. The MHR is distinct from the dimer interface and instead forms an intricate hydrogen-bonding network that interconnects strand 1 and helices 1 and 2. Alignment of the CA(146-231) dimer with the crystal structure of the capsid amino-terminal domain provides a model for the intact protein and extends models for assembly of the central conical core of HIV-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gamble, T R -- Yoo, S -- Vajdos, F F -- von Schwedler, U K -- Worthylake, D K -- Wang, H -- McCutcheon, J P -- Sundquist, W I -- Hill, C P -- R01 AI40333/AI/NIAID NIH HHS/ -- R01 AI43036/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 31;278(5339):849-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9346481" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Capsid/*chemistry/genetics ; Cell Line ; Cloning, Molecular ; Cloning, Organism ; Crystallography, X-Ray ; Dimerization ; HIV-1/*chemistry/genetics/physiology ; Humans ; Models, Molecular ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Peptidylprolyl Isomerase/chemistry ; *Protein Conformation ; Virus Replication
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    A critical role for tapasin in the assembly and function of multimeric MHC class I-TAP complexes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-29
    Description: Newly assembled major histocompatibility complex (MHC) class I molecules, together with the endoplasmic reticulum chaperone calreticulin, interact with the transporter associated with antigen processing (TAP) through a molecule called tapasin. The molecular cloning of tapasin revealed it to be a transmembrane glycoprotein encoded by an MHC-linked gene. It is a member of the immunoglobulin superfamily with a probable cytoplasmic endoplasmic reticulum retention signal. Up to four MHC class I-tapasin complexes were found to bind to each TAP molecule. Expression of tapasin in a negative mutant human cell line (220) restored class I-TAP association and normal class I cell surface expression. Tapasin expression also corrected the defective recognition of virus-infected 220 cells by class I-restricted cytotoxic T cells, establishing a critical functional role for tapasin in MHC class I-restricted antigen processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ortmann, B -- Copeman, J -- Lehner, P J -- Sadasivan, B -- Herberg, J A -- Grandea, A G -- Riddell, S R -- Tampe, R -- Spies, T -- Trowsdale, J -- Cresswell, P -- AI30581/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Aug 29;277(5330):1306-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9271576" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/*metabolism ; Amino Acid Sequence ; Antigen Presentation ; Antiporters/chemistry/genetics/*metabolism ; Calcium-Binding Proteins/metabolism ; Calreticulin ; Cell Line ; Cell Line, Transformed ; Chromosome Mapping ; Chromosomes, Human, Pair 6 ; Cloning, Molecular ; Dimerization ; Endoplasmic Reticulum/metabolism ; Genetic Linkage ; HLA Antigens/*metabolism ; Histocompatibility Antigens Class I/*metabolism ; Humans ; Immunoglobulin G/chemistry ; Immunoglobulins/chemistry/genetics/*metabolism ; Major Histocompatibility Complex/genetics ; Membrane Transport Proteins ; Molecular Sequence Data ; Ribonucleoproteins/metabolism ; Sequence Homology, Amino Acid ; T-Lymphocytes, Cytotoxic ; Tumor Cells, Cultured
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    Natural behavior polymorphism due to a cGMP-dependent protein kinase of Drosophila (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: Naturally occuring polymorphisms in behavior are difficult to map genetically and thus are refractory to molecular characterization. An exception is the foraging gene (for), a gene that has two naturally occurring variants in Drosophila melanogaster food-search behavior: rover and sitter. Molecular mapping placed for mutations in the dg2 gene, which encodes a cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG). Rovers had higher PKG activity than sitters, and transgenic sitters expressing a dg2 complementary DNA from rover showed transformation of behavior to rover. Thus, PKG levels affected food-search behavior, and natural variation in PKG activity accounted for a behavioral polymorphism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osborne, K A -- Robichon, A -- Burgess, E -- Butland, S -- Shaw, R A -- Coulthard, A -- Pereira, H S -- Greenspan, R J -- Sokolowski, M B -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):834-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, York University, 4700 Keele Street, North York, Toronto, Ontario, Canada, M3J 1P3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242616" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinases/*genetics/metabolism ; Drosophila melanogaster/*genetics/*physiology ; *Feeding Behavior ; *Genes, Insect ; Larva/genetics/physiology ; Phenotype ; Polymorphism, Genetic ; Signal Transduction
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    Inhibition of HIV-1 infection by the beta-chemokine MDC (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-24
    Description: CD8(+) T lymphocytes from individuals infected with human immunodeficiency virus-type 1 (HIV-1) secrete a soluble activity that suppresses infection by HIV-1. A protein associated with this activity was purified from the culture supernatant of an immortalized CD8(+) T cell clone and identified as the beta-chemokine macrophage-derived chemokine (MDC). MDC suppressed infection of CD8(+) cell-depleted peripheral blood mononuclear cells by primary non-syncytium-inducing and syncytium-inducing isolates of HIV-1 and the T cell line-adapted isolate HIV-1IIIB. MDC was expressed in activated, but not resting, peripheral blood mononuclear cells and binds a receptor on activated primary T cells. These observations indicate that beta-chemokines are responsible for a major proportion of HIV-1-specific suppressor activity produced by primary T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pal, R -- Garzino-Demo, A -- Markham, P D -- Burns, J -- Brown, M -- Gallo, R C -- DeVico, A L -- N01-AI-55279/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):695-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced BioScience Laboratories, 5510 Nicholson Lane, Kensington, MD 20895, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381181" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antiviral Agents/*immunology ; Blotting, Northern ; CD8-Positive T-Lymphocytes/*immunology ; Calcium/blood ; Cell Line ; Cell Line, Transformed ; Cells, Cultured ; Chemokine CCL22 ; Chemokines, CC/chemistry/*immunology/isolation & purification/metabolism ; HIV Core Protein p24/biosynthesis ; HIV Infections/immunology ; HIV-1/*immunology/physiology ; Humans ; Leukocytes, Mononuclear/immunology/metabolism/*virology ; Lymphocyte Activation ; Receptors, Chemokine/metabolism ; Receptors, HIV/metabolism ; T-Lymphocytes/immunology
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    Structure of a protein photocycle intermediate by millisecond time-resolved crystallography (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-07
    Description: The blue-light photoreceptor photoactive yellow protein (PYP) undergoes a self-contained light cycle. The atomic structure of the bleached signaling intermediate in the light cycle of PYP was determined by millisecond time-resolved, multiwavelength Laue crystallography and simultaneous optical spectroscopy. Light-induced trans-to-cis isomerization of the 4-hydroxycinnamyl chromophore and coupled protein rearrangements produce a new set of active-site hydrogen bonds. An arginine gateway opens, allowing solvent exposure and protonation of the chromophore's phenolic oxygen. Resulting changes in shape, hydrogen bonding, and electrostatic potential at the protein surface form a likely basis for signal transduction. The structural results suggest a general framework for the interpretation of protein photocycles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genick, U K -- Borgstahl, G E -- Ng, K -- Ren, Z -- Pradervand, C -- Burke, P M -- Srajer, V -- Teng, T Y -- Schildkamp, W -- McRee, D E -- Moffat, K -- Getzoff, E D -- GM36452/GM/NIGMS NIH HHS/ -- GM37684/GM/NIGMS NIH HHS/ -- RR07707/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1471-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045611" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*chemistry/physiology ; Binding Sites ; Chromatiaceae ; Crystallography, X-Ray ; Electrochemistry ; Hydrogen Bonding ; Isomerism ; Light ; Models, Molecular ; *Photoreceptors, Microbial ; *Protein Conformation ; Signal Transduction ; Spectrum Analysis
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    An antagonist decoy receptor and a death domain-containing receptor for TRAIL (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: TRAIL, also called Apo2L, is a cytotoxic protein that induces apoptosis of many transformed cell lines but not of normal tissues, even though its death domain-containing receptor, DR4, is expressed on both cell types. An antagonist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may explain the resistant phenotype of normal tissues was identified. TRID is a distinct gene product with an extracellular TRAIL-binding domain and a transmembrane domain but no intracellular signaling domain. TRID transcripts were detected in many normal human tissues but not in most cancer cell lines examined. Ectopic expression of TRID protected mammalian cells from TRAIL-induced apoptosis, which is consistent with a protective role. Another death domain-containing receptor for TRAIL (designated as death receptor-5), which preferentially engaged a FLICE (caspase-8)-related death protease, was also identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- Ni, J -- Wei, Y F -- Yu, G -- Gentz, R -- Dixit, V M -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):815-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242610" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caspase 10 ; Caspase 8 ; Caspase 9 ; *Caspases ; Cell Line, Transformed ; Cysteine Endopeptidases/metabolism ; GPI-Linked Proteins ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; Protein Sorting Signals ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Sequence Alignment ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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    Induction of cell migration by matrix metalloprotease-2 cleavage of laminin-5 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: Structural changes in the extracellular matrix are necessary for cell migration during tissue remodeling and tumor invasion. Specific cleavage of laminin-5 (Ln-5) by matrix metalloprotease-2 (MMP2) was shown to induce migration of breast epithelial cells. MMP2 cleaved the Ln-5 gamma2 subunit at residue 587, exposing a putative cryptic promigratory site on Ln-5 that triggers cell motility. This altered form of Ln-5 is found in tumors and in tissues undergoing remodeling, but not in quiescent tissues. Cleavage of Ln-5 by MMP2 and the resulting activation of the Ln-5 cryptic site may provide new targets for modulation of tumor cell invasion and tissue remodeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giannelli, G -- Falk-Marzillier, J -- Schiraldi, O -- Stetler-Stevenson, W G -- Quaranta, V -- CA47858/CA/NCI NIH HHS/ -- DE10063/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast/*cytology/metabolism ; Cell Adhesion ; Cell Adhesion Molecules/*metabolism ; Cell Division ; Cell Line ; *Cell Movement ; Cell Size ; Collagenases/metabolism ; Epithelial Cells ; Epithelium/metabolism ; Extracellular Matrix/*metabolism ; Female ; Fibrinolysin/metabolism ; Gelatinases/antagonists & inhibitors/*metabolism ; Humans ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; Metalloendopeptidases/antagonists & inhibitors/*metabolism ; Mice ; Phenylalanine/analogs & derivatives/pharmacology ; Protease Inhibitors/pharmacology ; Rats ; Recombinant Fusion Proteins/metabolism ; Skin Neoplasms/metabolism/pathology ; Thiophenes/pharmacology
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    Potent inhibition of HIV-1 infectivity in macrophages and lymphocytes by a novel CCR5 antagonist (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: The chemokine receptors CXCR4 and CCR5 have recently been shown to act as coreceptors, in concert with CD4, for human immunodeficiency virus-type 1 (HIV-1) infection. RANTES and other chemokines that interact with CCR5 and block infection of peripheral blood mononuclear cell cultures inhibit infection of primary macrophages inefficiently at best. If used to treat HIV-1-infected individuals, these chemokines could fail to influence HIV replication in nonlymphocyte compartments while promoting unwanted inflammatory side effects. A derivative of RANTES that was created by chemical modification of the amino terminus, aminooxypentane (AOP)-RANTES, did not induce chemotaxis and was a subnanomolar antagonist of CCR5 function in monocytes. It potently inhibited infection of diverse cell types (including macrophages and lymphocytes) by nonsyncytium-inducing, macrophage-tropic HIV-1 strains. Thus, activation of cells by chemokines is not a prerequisite for the inhibition of viral uptake and replication. Chemokine receptor antagonists like AOP-RANTES that achieve full receptor occupancy at nanomolar concentrations are strong candidates for the therapy of HIV-1-infected individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simmons, G -- Clapham, P R -- Picard, L -- Offord, R E -- Rosenkilde, M M -- Schwartz, T W -- Buser, R -- Wells, T N -- Proudfoot, A E -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virology Group, Chester Beatty Laboratories, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/metabolism ; Binding, Competitive ; Cats ; Cell Line ; Cells, Cultured ; Chemokine CCL4 ; Chemokine CCL5/metabolism/pharmacology ; Chemotaxis, Leukocyte ; HIV-1/*drug effects/physiology ; HeLa Cells ; Humans ; Macrophage Inflammatory Proteins/metabolism ; Macrophages/drug effects/*virology ; Receptors, CCR5 ; *Receptors, Chemokine ; Receptors, Cytokine/*antagonists & inhibitors/metabolism ; Receptors, HIV/*antagonists & inhibitors/metabolism ; T-Lymphocytes/drug effects/*virology ; Virus Replication/drug effects
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    The receptor for the cytotoxic ligand TRAIL (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: TRAIL (also known as Apo-2L) is a member of the tumor necrosis factor (TNF) ligand family that rapidly induces apoptosis in a variety of transformed cell lines. The human receptor for TRAIL was found to be an undescribed member of the TNF-receptor family (designated death receptor-4, DR4) that contains a cytoplasmic "death domain" capable of engaging the cell suicide apparatus but not the nuclear factor kappa B pathway in the system studied. Unlike Fas, TNFR-1, and DR3, DR4 could not use FADD to transmit the death signal, suggesting the use of distinct proximal signaling machinery. Thus, the DR4-TRAIL axis defines another receptor-ligand pair involved in regulating cell suicide and tissue homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- O'Rourke, K -- Chinnaiyan, A M -- Gentz, R -- Ebner, R -- Ni, J -- Dixit, V M -- DAMD17-96-1-6085/DA/NIDA NIH HHS/ -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):111-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082980" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Carrier Proteins/metabolism ; Cell Line ; Fas-Associated Death Domain Protein ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Proteins/metabolism ; RNA, Messenger/genetics/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/*metabolism
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    Maintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1 (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-06
    Description: In the absence of costimulation, T cells activated through their antigen receptor become unresponsive (anergic) and do not transcribe the gene encoding interleukin-2 (IL-2) when restimulated with antigen. Anergic alloantigen-specific human T cells contained phosphorylated Cbl that coimmunoprecipitated with Fyn. The adapter protein CrkL was associated with both phosphorylated Cbl and the guanidine nucleotide-releasing factor C3G, which catalyzes guanosine triphosphate (GTP) exchange on Rap1. Active Rap1 (GTP-bound form) was present in anergic cells. Forced expression of low amounts of Rap1-GTP in Jurkat T cells recapitulated the anergic defect and blocked T cell antigen receptor (TCR)- and CD28-mediated IL-2 gene transcription. Therefore, Rap1 functions as a negative regulator of TCR-mediated IL-2 gene transcription and may be responsible for the specific defect in IL-2 production in T cell anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boussiotis, V A -- Freeman, G J -- Berezovskaya, A -- Barber, D L -- Nadler, L M -- AI 35225/AI/NIAID NIH HHS/ -- AI39671/AI/NIAID NIH HHS/ -- HL 54785/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):124-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. vassiliki_boussiotis@macmailgw.dfci.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311917" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Antigens, CD28/immunology ; *Clonal Anergy ; GTP-Binding Proteins/*metabolism ; Gene Expression Regulation ; Guanine Nucleotide Exchange Factors ; Guanosine Triphosphate/metabolism ; Humans ; Interleukin-2/*genetics ; Jurkat Cells ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-cbl ; Proto-Oncogene Proteins c-fyn ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; *Transcription, Genetic ; Transfection ; *Ubiquitin-Protein Ligases ; rap GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors ; ras Proteins/metabolism ; src Homology Domains
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    Defective TNF-alpha-induced apoptosis in STAT1-null cells due to low constitutive levels of caspases (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Signal transducers and activators of transcription (STATs) enhance transcription of specific genes in response to cytokines and growth factors. STAT1 is also required for efficient constitutive expression of the caspases Ice, Cpp32, and Ich-1 in human fibroblasts. As a consequence, STAT1-null cells are resistant to apoptosis by tumor necrosis factor alpha (TNF-alpha). Reintroduction of STAT1alpha restored both TNF-alpha-induced apoptosis and the expression of Ice, Cpp32, and Ich-1. Variant STAT1 proteins carrying point mutations that inactivate domains required for STAT dimer formation nevertheless restored protease expression and sensitivity to apoptosis, indicating that the functions of STAT1 required for these activities are different from those that mediate induced gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, A -- Commane, M -- Flickinger, T W -- Horvath, C M -- Stark, G R -- P01 CA62220/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1630-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374464" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Caspase 1 ; Caspase 2 ; Caspase 3 ; *Caspases ; Cell Line ; Cysteine Endopeptidases/genetics/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dactinomycin/pharmacology ; Dimerization ; Gene Expression Regulation, Enzymologic ; Humans ; Interferon-gamma/pharmacology ; Phosphorylation ; Point Mutation ; Proteins/genetics/*metabolism ; STAT1 Transcription Factor ; Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
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    Modulation of Ras and a-factor function by carboxyl-terminal proteolysis (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-21
    Description: Prenylated proteins contain a covalently linked cholesterol intermediate near their carboxyl-termini. Maturation of most prenylated proteins involves proteolytic removal of the last three amino acids. Two genes in Saccharomyces cerevisiae, RCE1 and AFC1, were identified that appear to be responsible for this processing. The Afc1 protein is a zinc protease that participates in the processing of yeast a-factor mating pheromone. The Rce1 protein contributes to the processing of both Ras protein and a-factor. Deletion of both AFC1 and RCE1 resulted in the loss of proteolytic processing of prenylated proteins. Disruption of RCE1 led to defects in Ras localization and signaling and suppressed the activated phenotype associated with the allele RAS2val19.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyartchuk, V L -- Ashby, M N -- Rine, J -- GM35827/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1796-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065405" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane/metabolism ; Endopeptidases/chemistry/genetics/*metabolism ; Fungal Proteins/*metabolism ; Genes, Fungal ; Genes, ras ; Lipoproteins/*metabolism ; *Membrane Proteins ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mutation ; Pheromones ; Proprotein Convertases ; Protein Precursors/metabolism ; *Protein Prenylation ; *Protein Processing, Post-Translational ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Sequence Deletion ; Signal Transduction ; Substrate Specificity ; Zinc/pharmacology ; ras Proteins/*metabolism
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    Still life, a protein in synaptic terminals of Drosophila homologous to GDP-GTP exchangers (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-01-24
    Description: The morphology of axon terminals changes with differentiation into mature synapses. A molecule that might regulate this process was identified by a screen of Drosophila mutants for abnormal motor activities. The still life (sif) gene encodes a protein homologous to guanine nucleotide exchange factors, which convert Rho-like guanosine triphosphatases (GTPases) from a guanosine diphosphate-bound inactive state to a guanosine triphosphate-bound active state. The SIF proteins are found adjacent to the plasma membrane of synaptic terminals. Expression of a truncated SIF protein resulted in defects in neuronal morphology and induced membrane ruffling with altered actin localization in human KB cells. Thus, SIF proteins may regulate synaptic differentiation through the organization of the actin cytoskeleton by activating Rho-like GTPases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sone, M -- Hoshino, M -- Suzuki, E -- Kuroda, S -- Kaibuchi, K -- Nakagoshi, H -- Saigo, K -- Nabeshima, Y -- Hama, C -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):543-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, National Institute of Neuroscience (NIN), National Center of Neurology and Psychiatry (NCNP), Kodaira, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999801" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Amino Acid Sequence ; Animals ; Axons/physiology ; Cell Membrane/ultrastructure ; Cytoskeleton/physiology/ultrastructure ; DNA, Complementary/genetics ; Drosophila/embryology/genetics/*metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; GTP Phosphohydrolases/metabolism ; GTP-Binding Proteins/genetics/metabolism ; Gene Expression ; Genes, Insect ; *Guanine Nucleotide Exchange Factors ; Humans ; In Situ Hybridization ; KB Cells ; Molecular Sequence Data ; Movement ; Mutation ; Neuromuscular Junction/metabolism ; Presynaptic Terminals/*metabolism ; Signal Transduction ; *rac GTP-Binding Proteins
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    Beta-catenin as oncogene: the smoking gun (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peifer, M -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1752-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA. peifer@unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122680" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Apoptosis ; Cell Division ; Cell Movement ; Colon/cytology/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; DNA-Binding Proteins/metabolism ; *Drosophila Proteins ; Gene Expression Regulation, Neoplastic ; Genes, APC ; Humans ; Insect Proteins/metabolism ; Intestinal Mucosa/cytology/metabolism ; Lymphoid Enhancer-Binding Factor 1 ; Melanoma/*genetics/metabolism ; Mutation ; *Oncogenes ; *Repressor Proteins ; Signal Transduction ; *Trans-Activators ; Transcription Factors/metabolism ; Tumor Cells, Cultured ; beta Catenin
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: The Janus family of tyrosine kinases (JAK) plays an essential role in development and in coupling cytokine receptors to downstream intracellular signaling events. A t(9;12)(p24;p13) chromosomal translocation in a T cell childhood acute lymphoblastic leukemia patient was characterized and shown to fuse the 3' portion of JAK2 to the 5' region of TEL, a gene encoding a member of the ETS transcription factor family. The TEL-JAK2 fusion protein includes the catalytic domain of JAK2 and the TEL-specific oligomerization domain. TEL-induced oligomerization of TEL-JAK2 resulted in the constitutive activation of its tyrosine kinase activity and conferred cytokine-independent proliferation to the interleukin-3-dependent Ba/F3 hematopoietic cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacronique, V -- Boureux, A -- Valle, V D -- Poirel, H -- Quang, C T -- Mauchauffe, M -- Berthou, C -- Lessard, M -- Berger, R -- Ghysdael, J -- Bernard, O A -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U 301 de l'Institut National de la Sante et de la Recherche Medicale and SD 401 No. 301 CNRS, Institut de Genetique Moleculaire, 27 rue Juliette Dodu, 75010 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360930" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biopolymers ; Cell Division ; Cell Line ; Child, Preschool ; DNA-Binding Proteins/chemistry/genetics/metabolism ; Enzyme Activation ; Humans ; Interleukin-3/physiology ; Janus Kinase 2 ; Leukemia-Lymphoma, Adult T-Cell/genetics/*metabolism ; Male ; Mice ; *Milk Proteins ; Molecular Sequence Data ; Oncogene Proteins, Fusion/chemistry/genetics/*metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/chemistry/genetics/*metabolism ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-ets ; *Repressor Proteins ; STAT5 Transcription Factor ; Signal Transduction ; Trans-Activators/metabolism ; Transcription Factors/chemistry/genetics/metabolism ; Transfection ; Translocation, Genetic
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    Controlling cell death (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golstein, P -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1081-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie INSERM-CNRS de Marseille-Luminy, France. golstein@ciml.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caenorhabditis elegans/cytology/metabolism ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/metabolism ; Caspase 1 ; *Caspases ; Cysteine Endopeptidases/metabolism ; Cytochrome c Group/metabolism ; Cytosol/metabolism ; Helminth Proteins/metabolism ; Membrane Glycoproteins/metabolism ; Mitochondria/metabolism ; Perforin ; Pore Forming Cytotoxic Proteins ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction ; Transfection ; bcl-X Protein
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  • 74
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    Tyrosine phosphorylation of transmembrane ligands for Eph receptors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: Axonal pathfinding in the nervous system is mediated in part by cell-to-cell signaling events involving members of the Eph receptor tyrosine kinase (RTK) family and their membrane-bound ligands. Genetic evidence suggests that transmembrane ligands may transduce signals in the developing embryo. The cytoplasmic domain of the transmembrane ligand Lerk2 became phosphorylated on tyrosine residues after contact with the Nuk/Cek5 receptor ectodomain, which suggests that Lerk2 has receptorlike intrinsic signaling potential. Moreover, Lerk2 is an in vivo substrate for the platelet-derived growth factor receptor, which suggests crosstalk between Lerk2 signaling and signaling cascades activated by tyrosine kinases. It is proposed that transmembrane ligands of Eph receptors act not only as conventional RTK ligands but also as receptorlike signaling molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruckner, K -- Pasquale, E B -- Klein, R -- EY10576/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1640-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054357" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Axons/physiology ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Membrane/*metabolism ; Embryo, Mammalian/metabolism ; Ephrin-B1 ; Ligands ; Mice ; Phosphorylation ; Phosphotyrosine/*metabolism ; Platelet-Derived Growth Factor/pharmacology ; Proteins/*metabolism/pharmacology ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, Ciliary Neurotrophic Factor ; Receptor, EphB2 ; Receptors, Nerve Growth Factor/metabolism ; Receptors, Platelet-Derived Growth Factor/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: The immunosuppressant rapamycin interferes with G1-phase progression in lymphoid and other cell types by inhibiting the function of the mammalian target of rapamycin (mTOR). mTOR was determined to be a terminal kinase in a signaling pathway that couples mitogenic stimulation to the phosphorylation of the eukaryotic initiation factor (eIF)-4E-binding protein, PHAS-I. The rapamycin-sensitive protein kinase activity of mTOR was required for phosphorylation of PHAS-I in insulin-stimulated human embryonic kidney cells. mTOR phosphorylated PHAS-I on serine and threonine residues in vitro, and these modifications inhibited the binding of PHAS-I to eIF-4E. These studies define a role for mTOR in translational control and offer further insights into the mechanism whereby rapamycin inhibits G1-phase progression in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunn, G J -- Hudson, C C -- Sekulic, A -- Williams, J M -- Hosoi, H -- Houghton, P J -- Lawrence, J C Jr -- Abraham, R T -- AR41189/AR/NIAMS NIH HHS/ -- DK28312/DK/NIDDK NIH HHS/ -- DK50628/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):99-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204908" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Androstadienes/pharmacology ; Animals ; Carrier Proteins/pharmacology ; Cell Line ; DNA-Binding Proteins/pharmacology ; Eukaryotic Initiation Factor-4E ; G1 Phase ; Heat-Shock Proteins/pharmacology ; Humans ; Insulin/pharmacology ; Peptide Initiation Factors/metabolism ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Polyenes/*pharmacology ; *Protein Kinases ; Rats ; Recombinant Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Sirolimus ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    What makes fruit flies roam? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):763-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Cyclic GMP-Dependent Protein Kinases/*genetics/metabolism ; Drosophila/*genetics/physiology ; Feeding Behavior ; *Genes, Insect ; Larva/genetics/physiology ; Mutagenesis, Insertional ; Signal Transduction
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    A Myc-induced apoptosis pathway surfaces (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, D R -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1246-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA. dgreen5240@aol.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411752" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis ; Carrier Proteins/metabolism ; Caspase 1 ; Cysteine Endopeptidases/metabolism ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Genes, Tumor Suppressor ; Genes, myc ; Genes, p53 ; Membrane Glycoproteins/genetics/*metabolism ; Ornithine Decarboxylase/metabolism ; Proto-Oncogene Proteins c-myc/*metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Differential effects of cytolytic T cell subsets on intracellular infection (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: In analyzing mechanisms of protection against intracellular infections, a series of human CD1-restricted T cell lines of two distinct phenotypes were derived. Both CD4(-)CD8(-) (double-negative) T cells and CD8(+) T cells efficiently lysed macrophages infected with Mycobacterium tuberculosis. The cytotoxicity of CD4(-)CD8(-) T cells was mediated by Fas-FasL interaction and had no effect on the viability of the mycobacteria. The CD8(+) T cells lysed infected macrophages by a Fas-independent, granule-dependent mechanism that resulted in killing of bacteria. These data indicate that two phenotypically distinct subsets of human cytolytic T lymphocytes use different mechanisms to kill infected cells and contribute in different ways to host defense against intracellular infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenger, S -- Mazzaccaro, R J -- Uyemura, K -- Cho, S -- Barnes, P F -- Rosat, J P -- Sette, A -- Brenner, M B -- Porcelli, S A -- Bloom, B R -- Modlin, R L -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1684-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California Los Angeles School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180075" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD1/*immunology ; Antigens, CD95/immunology/metabolism ; Cell Line ; Coculture Techniques ; Colony Count, Microbial ; Cytoplasmic Granules/immunology ; *Cytotoxicity, Immunologic ; Fas Ligand Protein ; Granzymes ; Humans ; Lymphocyte Activation ; Macrophages/*immunology/microbiology ; Membrane Glycoproteins/genetics/immunology/metabolism ; Mycobacterium tuberculosis/growth & development/*immunology ; Perforin ; Phenotype ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/metabolism ; Strontium/pharmacology ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Cytotoxic/*immunology
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    The transcriptional paradox: octamer factors and B and T cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graef, I A -- Crabtree, G R -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):193-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford Medical School, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235633" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*metabolism ; DNA-Binding Proteins/*metabolism ; Homeodomain Proteins/*metabolism ; Host Cell Factor C1 ; Interleukin-2/genetics ; Lymphocyte Activation ; Mice ; Octamer Transcription Factor-1 ; Octamer Transcription Factor-2 ; Signal Transduction ; T-Lymphocytes/*metabolism ; Trans-Activators/*metabolism ; Transcription Factors/*metabolism ; *Transcription, Genetic
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  • 80
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    Dual role of phosphatidylinositol-3,4,5-trisphosphate in the activation of protein kinase B (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: Protein kinase B (PKB) is a proto-oncogene that is activated in signaling pathways initiated by phosphoinositide 3-kinase. Chromatographic separation of brain cytosol revealed a kinase activity that phosphorylated and activated PKB only in the presence of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P3]. Phosphorylation occurred exclusively on threonine-308, a residue implicated in activation of PKB in vivo. PtdIns(3,4,5)P3 was determined to have a dual role: Its binding to the pleckstrin homology domain of PKB was required to allow phosphorylation by the upstream kinase and it directly activated the upstream kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokoe, D -- Stephens, L R -- Copeland, T -- Gaffney, P R -- Reese, C B -- Painter, G F -- Holmes, A B -- McCormick, F -- Hawkins, P T -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):567-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, 3031 Research Drive, Richmond, CA 94806, USA. stokoe@cc.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228007" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Blood Proteins/chemistry ; Brain/enzymology ; COS Cells ; Cytosol/enzymology ; Enzyme Activation ; Humans ; Male ; Molecular Sequence Data ; Phosphatidylinositol Phosphates/*metabolism ; *Phosphoproteins ; Phosphorylation ; Phosphothreonine/metabolism ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Stereoisomerism
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    Regulation of NF-kappaB by cyclin-dependent kinases associated with the p300 coactivator (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-24
    Description: The nuclear factor kappaB (NF-kappaB) transcription factor is responsive to specific cytokines and stress and is often activated in association with cell damage and growth arrest in eukaryotes. NF-kappaB is a heterodimeric protein, typically composed of 50- and 65-kilodalton subunits of the Rel family, of which RelA(p65) stimulates transcription of diverse genes. Specific cyclin-dependent kinases (CDKs) were found to regulate transcriptional activation by NF-kappaB through interactions with the coactivator p300. The transcriptional activation domain of RelA(p65) interacted with an amino-terminal region of p300 distinct from a carboxyl-terminal region of p300 required for binding to the cyclin E-Cdk2 complex. The CDK inhibitor p21 or a dominant negative Cdk2, which inhibited p300-associated cyclin E-Cdk2 activity, stimulated kappaB-dependent gene expression, which was also enhanced by expression of p300 in the presence of p21. The interaction of NF-kappaB and CDKs through the p300 and CBP coactivators provides a mechanism for the coordination of transcriptional activation with cell cycle progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perkins, N D -- Felzien, L K -- Betts, J C -- Leung, K -- Beach, D H -- Nabel, G J -- R01 AI29179/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical Center, 4520 MSRB I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999795" target="_blank"〉PubMed〈/a〉
    Keywords: *CDC2-CDC28 Kinases ; Cell Cycle ; Cell Line ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/genetics/*metabolism ; Cyclins/genetics/metabolism ; Genes, Reporter ; Humans ; Jurkat Cells ; NF-kappa B/genetics/*metabolism ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; *Trans-Activators ; Transcription Factor RelA ; Transcription Factors/genetics/*metabolism ; *Transcriptional Activation ; Transfection
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    Specific inhibition of Stat3 signal transduction by PIAS3 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: The signal transducer and activator of transcription-3 (Stat3) protein is activated by the interleukin 6 (IL-6) family of cytokines, epidermal growth factor, and leptin. A protein named PIAS3 (protein inhibitor of activated STAT) that binds to Stat3 was isolated and characterized. The association of PIAS3 with Stat3 in vivo was only observed in cells stimulated with ligands that cause the activation of Stat3. PIAS3 blocked the DNA-binding activity of Stat3 and inhibited Stat3-mediated gene activation. Although Stat1 is also phosphorylated in response to IL-6, PIAS3 did not interact with Stat1 or affect its DNA-binding or transcriptional activity. The results indicate that PIAS3 is a specific inhibitor of Stat3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, C D -- Liao, J -- Liu, B -- Rao, X -- Jay, P -- Berta, P -- Shuai, K -- AI39612/AI/NIAID NIH HHS/ -- T32CA09056/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Dec 5;278(5344):1803-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9388184" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism/pharmacology ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation ; Humans ; Interferon Regulatory Factor-1 ; Interferon-alpha/pharmacology ; Interleukin-6/pharmacology ; *Intracellular Signaling Peptides and Proteins ; Mice ; Molecular Sequence Data ; NF-kappa B/metabolism ; Phosphoproteins/genetics ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Inhibitors of Activated STAT ; Recombinant Fusion Proteins/pharmacology ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/*metabolism ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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    Fishing for answers to whirling disease (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potera, C -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):225-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryota/*growth & development/isolation & purification ; Fish Diseases/diagnosis/*parasitology ; Fisheries ; Montana ; Oligochaeta/parasitology ; Oncorhynchus mykiss/*parasitology ; Polymerase Chain Reaction ; Protozoan Infections/diagnosis/parasitology ; *Protozoan Infections, Animal ; RNA, Protozoan/genetics ; RNA, Ribosomal/genetics ; Spores/physiology ; Temperature
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    Combinatorial control required for the specificity of yeast MAPK signaling (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-28
    Description: In yeast, an overlapping set of mitogen-activated protein kinase (MAPK) signaling components controls mating, haploid invasion, and pseudohyphal development. Paradoxically, a single downstream transcription factor, Ste12, is necessary for the execution of these distinct programs. Developmental specificity was found to require a transcription factor of the TEA/ATTS family, Tec1, which cooperates with Ste12 during filamentous and invasive growth. Purified derivatives of Ste12 and Tec1 bind cooperatively to enhancer elements called filamentation and invasion response elements (FREs), which program transcription that is specifically responsive to the MAPK signaling components required for filamentous growth. An FRE in the TEC1 promoter functions in a positive feedback loop required for pseudohyphal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Madhani, H D -- Fink, G R -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036858" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; *Enhancer Elements, Genetic ; Fungal Proteins/*metabolism ; Intracellular Signaling Peptides and Proteins ; MAP Kinase Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinase Kinases ; Mutation ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Retroelements ; Saccharomyces cerevisiae/genetics/growth & development/*metabolism ; *Saccharomyces cerevisiae Proteins ; *Schizosaccharomyces pombe Proteins ; Signal Transduction ; *Transcription Factors ; Transcription, Genetic
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  • 85
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    SBF cell cycle regulator as a target of the yeast PKC-MAP kinase pathway (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-21
    Description: Protein kinase C (PKC) signaling is highly conserved among eukaryotes and has been implicated in the regulation of cellular processes such as cell proliferation and growth. In the budding yeast, PKC1 functions to activate the SLT2(MPK1) mitogen-activated protein (MAP) kinase cascade, which is required for the maintenance of cell integrity during asymmetric cell growth. Genetic studies, coimmunoprecipitation experiments, and analysis of protein phosphorylation in vivo and in vitro indicate that the SBF transcription factor (composed of Swi4p and Swi6p), an important regulator of gene expression at the G1 to S phase cell cycle transition, is a target of the Slt2p(Mpk1p) MAP kinase. These studies provide evidence for a direct role of the PKC1 pathway in the regulation of the yeast cell cycle and cell growth and indicate that conserved signaling pathways can act to control key regulators of cell division.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Madden, K -- Sheu, Y J -- Baetz, K -- Andrews, B -- Snyder, M -- GM36494/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1781-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Yale University, Post Office Box 208103, New Haven, CT 06520-8103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065400" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; *Cell Cycle ; Cyclins/genetics ; Fungal Proteins/genetics/*metabolism ; G1 Phase ; Gene Expression Regulation, Fungal ; *Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinase C/genetics/*metabolism ; S Phase ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; Transformation, Genetic ; Yeasts/cytology/genetics/growth & development/*metabolism
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  • 86
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    Preserved acute pain and reduced neuropathic pain in mice lacking PKCgamma (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-10
    Description: In normal animals, peripheral nerve injury produces a persistent, neuropathic pain state in which pain is exaggerated and can be produced by nonpainful stimuli. Here, mice that lack protein kinase C gamma (PKCgamma) displayed normal responses to acute pain stimuli, but they almost completely failed to develop a neuropathic pain syndrome after partial sciatic nerve section, and the neurochemical changes that occurred in the spinal cord after nerve injury were blunted. Also, PKCgamma was shown to be restricted to a small subset of dorsal horn neurons, thus identifying a potential biochemical target for the prevention and therapy of persistent pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malmberg, A B -- Chen, C -- Tonegawa, S -- Basbaum, A I -- DA08377/DA/NIDA NIH HHS/ -- NS 14627/NS/NINDS NIH HHS/ -- NS 21445/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):279-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco, CA 92143, USA. annikam@phy.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ganglia, Spinal/metabolism ; Gene Deletion ; Hyperalgesia/physiopathology/*therapy ; Inflammation/physiopathology/therapy ; Interneurons/*enzymology ; Isoenzymes/deficiency/genetics/*metabolism ; Ligation ; Mice ; Mice, Knockout ; Neuropeptide Y/metabolism ; Pain/physiopathology ; *Pain Management ; Pain Threshold ; Protein Kinase C/deficiency/genetics/*metabolism ; Receptors, Neurokinin-1/metabolism ; Sciatic Nerve/surgery ; Signal Transduction ; Spinal Cord/cytology/*enzymology/metabolism ; Substance P/metabolism
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  • 87
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    Inhibition of invasion of epithelial cells by Tiam1-Rac signaling (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Tiam1 encodes an exchange factor for the Rho-like guanosine triphosphatase Rac. Both Tiam1 and activated RacV12 promote invasiveness of T lymphoma cells. In epithelial Madin-Darby canine kidney (MDCK) cells, Tiam1 localized to adherens junctions. Ectopic expression of Tiam1 or RacV12 inhibited hepatocyte growth factor-induced scattering by increasing E-cadherin-mediated cell-cell adhesion accompanied by actin polymerization at cell-cell contacts. In Ras-transformed MDCK cells, expression of Tiam1 or RacV12 restored E-cadherin-mediated adhesion, resulting in phenotypic reversion and loss of invasiveness. These data suggest an invasion-suppressor role for Tiam1 and Rac in epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hordijk, P L -- ten Klooster, J P -- van der Kammen, R A -- Michiels, F -- Oomen, L C -- Collard, J G -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1464-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9367959" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Cadherins/metabolism ; *Cell Adhesion ; Cell Line ; Cell Line, Transformed ; Cell Movement ; Cell Transformation, Neoplastic ; Cytoplasm/metabolism ; Epithelial Cells/*cytology/metabolism ; GTP-Binding Proteins/*metabolism ; Hepatocyte Growth Factor/pharmacology ; Intercellular Junctions/*metabolism ; *Neoplasm Invasiveness ; Phenotype ; Proteins/genetics/*metabolism ; Signal Transduction ; rac GTP-Binding Proteins
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  • 88
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    An NGF-TrkA-mediated retrograde signal to transcription factor CREB in sympathetic neurons (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: Nerve growth factor (NGF) is a neurotrophic factor secreted by cells that are the targets of innervation of sympathetic and some sensory neurons. However, the mechanism by which the NGF signal is propagated from the axon terminal to the cell body, which can be more than 1 meter away, to influence biochemical events critical for growth and survival of neurons has remained unclear. An NGF-mediated signal transmitted from the terminals and distal axons of cultured rat sympathetic neurons to their nuclei regulated phosphorylation of the transcription factor CREB (cyclic adenosine monophosphate response element-binding protein). Internalization of NGF and its receptor tyrosine kinase TrkA, and their transport to the cell body, were required for transmission of this signal. The tyrosine kinase activity of TrkA was required to maintain it in an autophosphorylated state upon its arrival in the cell body and for propagation of the signal to CREB within neuronal nuclei. Thus, an NGF-TrkA complex is a messenger that delivers the NGF signal from axon terminals to cell bodies of sympathetic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riccio, A -- Pierchala, B A -- Ciarallo, C L -- Ginty, D D -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1097-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; *Axonal Transport ; Axons/*metabolism ; Carbazoles/pharmacology ; Cell Membrane/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/*metabolism ; Indole Alkaloids ; Microspheres ; Nerve Growth Factors/*metabolism/pharmacology ; Neurons/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/antagonists & inhibitors/*metabolism ; Signal Transduction ; Superior Cervical Ganglion/cytology
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  • 89
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    A G protein-coupled receptor phosphatase required for rhodopsin function (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-08-01
    Description: Heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors are phosphorylated by kinases that mediate agonist-dependent receptor deactivation. Although many receptor kinases have been isolated, the corresponding phosphatases, necessary for restoring the ground state of the receptor, have not been identified. Drosophila RDGC (retinal degeneration C) is a phosphatase required for rhodopsin dephosphorylation in vivo. Loss of RDGC caused severe defects in the termination of the light response as well as extensive light-dependent retinal degeneration. These phenotypes resulted from the hyperphosphorylation of rhodopsin because expression of a truncated rhodopsin lacking the phosphorylation sites restored normal photoreceptor function. These results suggest the existence of a family of receptor phosphatases involved in the regulation of G protein-coupled signaling cascades.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vinos, J -- Jalink, K -- Hardy, R W -- Britt, S G -- Zuker, C S -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):687-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biology, University of California at San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Arrestin/metabolism ; *Calcium-Binding Proteins ; Darkness ; Drosophila ; *Drosophila Proteins ; Electroretinography ; GTP-Binding Proteins/*metabolism ; Light ; Mutation ; Phosphoprotein Phosphatases/genetics/*metabolism ; Phosphorylation ; Photoreceptor Cells, Invertebrate/*metabolism ; Retina/metabolism ; Retinal Degeneration ; Rhodopsin/*metabolism ; Signal Transduction
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  • 90
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    Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-11-21
    Description: Induction of apoptosis by oncogenes like c-myc may be important in restraining the emergence of neoplasia. However, the mechanism by which c-myc induces apoptosis is unknown. CD95 (also termed Fas or APO-1) is a cell surface transmembrane receptor of the tumor necrosis factor receptor family that activates an intrinsic apoptotic suicide program in cells upon binding either its ligand CD95L or antibody. c-myc-induced apoptosis was shown to require interaction on the cell surface between CD95 and its ligand. c-Myc acts downstream of the CD95 receptor by sensitizing cells to the CD95 death signal. Moreover, IGF-I signaling and Bcl-2 suppress c-myc-induced apoptosis by also acting downstream of CD95. These findings link two apoptotic pathways previously thought to be independent and establish the dependency of Myc on CD95 signaling for its killing activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hueber, A O -- Zornig, M -- Lyon, D -- Suda, T -- Nagata, S -- Evan, G I -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1305-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial Cancer Research Fund (ICRF) Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360929" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/*metabolism ; *Apoptosis ; Autocrine Communication ; Carrier Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Gene Expression Regulation ; Genes, myc ; Insulin-Like Growth Factor I/pharmacology/physiology ; Membrane Glycoproteins/*metabolism ; Mice ; Proto-Oncogene Proteins c-bcl-2/pharmacology/physiology ; Proto-Oncogene Proteins c-myc/*metabolism ; Rats
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  • 91
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    Common and distinct roles of DFos and DJun during Drosophila development (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-24
    Description: The Drosophila homolog of c-Jun regulates epithelial cell shape changes during the process of dorsal closure in mid-embryogenesis. Here, mutations in the DFos gene are described. In dorsal closure, DFos cooperates with DJun by regulating the expression of dpp; Dpp acts as a relay signal that triggers cell shape changes and DFos expression in neighboring cells. In addition to the joint requirement of DFos and DJun during dorsal closure, DFos functions independently of DJun during early stages of embryogenesis. These findings demonstrate common and distinct roles of DFos and DJun during embryogenesis and suggest a conserved link between AP-1 (activating protein-1) and TGF-beta (transforming growth factor-beta) signaling during epithelial cell shape changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riesgo-Escovar, J R -- Hafen, E -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):669-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoologisches Institut, Universitat Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381174" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Size ; Dimerization ; Drosophila/*embryology/genetics/metabolism ; *Drosophila Proteins ; Ectoderm/metabolism ; Endoderm/metabolism ; Epithelial Cells/cytology/metabolism ; Gene Expression Regulation, Developmental ; Genes, Insect ; Genes, fos ; Genes, jun ; Homeodomain Proteins/genetics ; Insect Proteins/genetics/physiology ; *JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; Metamorphosis, Biological ; *Mitogen-Activated Protein Kinase Kinases ; Mutation ; Peptidyl-Dipeptidase A/genetics ; Phenotype ; Point Mutation ; Protein Kinases/genetics/metabolism ; Proto-Oncogene Proteins c-fos/*physiology ; Proto-Oncogene Proteins c-jun/*physiology ; Signal Transduction ; Transcription Factor AP-1/metabolism ; Transforming Growth Factor beta/genetics/metabolism
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  • 92
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    Good pain, bad pain (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iadarola, J M -- Caudle, R M -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):239-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pain and Neurosensory Mechanisms Branch, National Institute of Dental Research, NIH, Bethesda, MD 20892-4410, USA. iadarola@yoda.nidr.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340772" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Humans ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Isoenzymes/genetics/*metabolism ; Mice ; Mutation ; *N-Glycosyl Hydrolases ; Neuronal Plasticity ; Neurons/*metabolism/pathology ; Pain/physiopathology ; *Pain Management ; Plant Proteins/*administration & dosage ; Protein Kinase C/genetics/*metabolism ; Rats ; Receptors, Neurokinin-1/biosynthesis ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord ; Substance P/administration & dosage
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  • 93
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    Antigen presentation by memory B cells: the sting is in the tail (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tarlinton, D -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):374-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia. tarlinton@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139358" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; B-Lymphocytes/*immunology ; Cytoplasm ; Endosomes/immunology ; Gene Targeting ; Genes, Immunoglobulin ; Humans ; Immunoglobulin Class Switching ; *Immunologic Memory ; Mice ; Receptors, Antigen, B-Cell/biosynthesis/chemistry/*immunology ; Signal Transduction ; T-Lymphocytes/immunology
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  • 94
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    Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-01-03
    Description: Mitogen-activated protein (MAP) kinase cascades are activated in response to various extracellular stimuli, including growth factors and environmental stresses. A MAP kinase kinase kinase (MAPKKK), termed ASK1, was identified that activated two different subgroups of MAP kinase kinases (MAPKK), SEK1 (or MKK4) and MKK3/MAPKK6 (or MKK6), which in turn activated stress-activated protein kinase (SAPK, also known as JNK; c-Jun amino-terminal kinase) and p38 subgroups of MAP kinases, respectively. Overexpression of ASK1 induced apoptotic cell death, and ASK1 was activated in cells treated with tumor necrosis factor-alpha (TNF-alpha). Moreover, TNF-alpha-induced apoptosis was inhibited by a catalytically inactive form of ASK1. ASK1 may be a key element in the mechanism of stress- and cytokine-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ichijo, H -- Nishida, E -- Irie, K -- ten Dijke, P -- Saitoh, M -- Moriguchi, T -- Takagi, M -- Matsumoto, K -- Miyazono, K -- Gotoh, Y -- New York, N.Y. -- Science. 1997 Jan 3;275(5296):90-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, The Cancer Institute, Tokyo, Japanese Foundation for Cancer Research, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8974401" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Division ; Cell Line ; Cell Survival ; Enzyme Activation ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 6 ; MAP Kinase Kinase Kinases ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; *Signal Transduction ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; p38 Mitogen-Activated Protein Kinases
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  • 95
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    Effect of transmembrane and cytoplasmic domains of IgE on the IgE response (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-04-18
    Description: B cells use immunoglobulin M (IgM) and IgD as antigen receptors, but after contact with antigen they can switch and use IgG, IgA, or IgE. In mice lacking the transmembrane and cytoplasmic domains of IgE, serum IgE is reduced by more than 95 percent and, after immunization, specific responses are negligible. In mice lacking most of the cytoplasmic tail of IgE, serum IgE levels are reduced by 50 percent and specific responses are reduced by 40 to 80 percent, without a clear secondary response. Thus, membrane expression is indispensable for IgE secretion in vivo, and the cytoplasmic tail influences the degree and quality of the response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Achatz, G -- Nitschke, L -- Lamers, M C -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):409-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Immunbiologie, Stubeweg 51, D-79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103198" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody-Producing Cells/immunology ; *Antigen Presentation ; Cytoplasm ; Dimerization ; Female ; Gene Targeting ; Immunization ; Immunoglobulin Class Switching ; Immunoglobulin E/blood/chemistry/genetics/*immunology ; Immunoglobulin G/blood ; Immunologic Memory ; Male ; Mice ; Mutation ; Nippostrongylus ; Receptors, Antigen, B-Cell/*immunology ; Signal Transduction ; Strongylida Infections/immunology ; Th2 Cells/immunology
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  • 96
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    Binding of neuroligins to PSD-95 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: PSD-95 is a component of postsynaptic densities in central synapses. It contains three PDZ domains that localize N-methyl-D-aspartate receptor subunit 2 (NMDA2 receptor) and K+ channels to synapses. In mouse forebrain, PSD-95 bound to the cytoplasmic COOH-termini of neuroligins, which are neuronal cell adhesion molecules that interact with beta-neurexins and form intercellular junctions. Neuroligins bind to the third PDZ domain of PSD-95, whereas NMDA2 receptors and K+ channels interact with the first and second PDZ domains. Thus different PDZ domains of PSD-95 are specialized for distinct functions. PSD-95 may recruit ion channels and neurotransmitter receptors to intercellular junctions formed between neurons by neuroligins and beta-neurexins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Irie, M -- Hata, Y -- Takeuchi, M -- Ichtchenko, K -- Toyoda, A -- Hirao, K -- Takai, Y -- Rosahl, T W -- Sudhof, T C -- R01-MH52804/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1511-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Takai Biotimer Project, ERATO, Japan Science and Technology Corporation, 2-2-10, Murotani, Nishi-ku, Kobe, 651-22, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278515" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; COS Cells ; *Calcium-Calmodulin-Dependent Protein Kinases ; Cell Adhesion Molecules, Neuronal ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Guanylate Kinase ; Intercellular Junctions/metabolism ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurons/*metabolism ; Nucleoside-Phosphate Kinase/metabolism ; Potassium Channels/metabolism ; Prosencephalon/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Mitogenic signaling mediated by oxidants in Ras-transformed fibroblasts (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: NIH 3T3 fibroblasts stably transformed with a constitutively active isoform of p21(Ras), H-RasV12 (v-H-Ras or EJ-Ras), produced large amounts of the reactive oxygen species superoxide (.O2-). .O2- production was suppressed by the expression of dominant negative isoforms of Ras or Rac1, as well as by treatment with a farnesyltransferase inhibitor or with diphenylene iodonium, a flavoprotein inhibitor. The mitogenic activity of cells expressing H-RasV12 was inhibited by treatment with the chemical antioxidant N-acetyl-L-cysteine. Mitogen-activated protein kinase (MAPK) activity was decreased and c-Jun N-terminal kinase (JNK) was not activated in H-RasV12-transformed cells. Thus, H-RasV12-induced transformation can lead to the production of .O2- through one or more pathways involving a flavoprotein and Rac1. The implication of a reactive oxygen species, probably .O2-, as a mediator of Ras-induced cell cycle progression independent of MAPK and JNK suggests a possible mechanism for the effects of antioxidants against Ras-induced cellular transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Irani, K -- Xia, Y -- Zweier, J L -- Sollott, S J -- Der, C J -- Fearon, E R -- Sundaresan, M -- Finkel, T -- Goldschmidt-Clermont, P J -- HL52315/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1649-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054359" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Acetylcysteine/pharmacology ; Animals ; Antioxidants/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; *Cell Cycle ; Cell Line, Transformed ; *Cell Transformation, Neoplastic ; DNA/biosynthesis ; Electron Spin Resonance Spectroscopy ; GTP-Binding Proteins/metabolism ; *Genes, ras ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Oxidation-Reduction ; Proto-Oncogene Proteins p21(ras)/genetics/*metabolism ; Reactive Oxygen Species/*metabolism ; Signal Transduction ; Superoxides/*metabolism ; Transfection ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Activation of the G protein Gq/11 through tyrosine phosphorylation of the alpha subunit (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: Various receptors coupled to the heterotrimeric guanine nucleotide-binding protein Gq/11 stimulate formation of inositol-1,4,5-trisphosphate (IP3). Activation of these receptors also induces protein tyrosine phosphorylation. Formation of IP3 in response to stimulated receptors that couple to Gq/11 was blocked by protein tyrosine kinase inhibitors. These inhibitors appeared to act before activation of Gq/11. Moreover, stimulation of receptors coupled to Gq/11 induced phosphorylation on a tyrosine residue (Tyr356) of the Galphaq/11 subunit, and this tyrosine phosphorylation event was essential for Gq/11 activation. Tyrosine phosphorylation of Galphaq/11 induced changes in its interaction with receptors. Therefore, tyrosine phosphorylation of Galphaq/11 appears to regulate the activation of Gq/11 protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umemori, H -- Inoue, T -- Kume, S -- Sekiyama, N -- Nagao, M -- Itoh, H -- Nakanishi, S -- Mikoshiba, K -- Yamamoto, T -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1878-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Calcium/metabolism ; Carbachol/pharmacology ; Cell Line ; Cricetinae ; Enzyme Inhibitors/pharmacology ; GTP-Binding Proteins/*metabolism ; Genistein ; Inositol 1,4,5-Trisphosphate/metabolism ; Isoflavones/pharmacology ; Phosphorylation ; Phosphotyrosine/*metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Receptors, Cholinergic/*metabolism ; Receptors, Metabotropic Glutamate/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    A new player in cell death (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoey, T -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1578-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, South San Francisco, CA 94080, USA. hoey@tularik.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411781" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Caspase 1 ; Cell Line ; Cysteine Endopeptidases/metabolism ; DNA-Binding Proteins/chemistry/genetics/metabolism/*physiology ; Gene Expression Regulation ; Gene Expression Regulation, Enzymologic ; Humans ; Interferon Regulatory Factor-1 ; Interferon-gamma/pharmacology ; Models, Genetic ; Mutation ; Phosphoproteins/metabolism ; Phosphorylation ; STAT1 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/genetics/*physiology ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Inhibition of hyperalgesia by ablation of lamina I spinal neurons expressing the substance P receptor (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: Substance P is released in the spinal cord in response to painful stimuli, but its role in nociceptive signaling remains unclear. When a conjugate of substance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was internalized and cytotoxic to lamina I spinal cord neurons that express the substance P receptor. This treatment left responses to mild noxious stimuli unchanged, but markedly attenuated responses to highly noxious stimuli and mechanical and thermal hyperalgesia. Thus, lamina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmission of highly noxious stimuli and the maintenance of hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- Rogers, S D -- Honore, P -- Allen, B J -- Ghilardi, J R -- Li, J -- Daughters, R S -- Lappi, D A -- Wiley, R G -- Simone, D A -- MH56368/MH/NIMH NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- NS31223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory (151), Veterans Administration Medical Center, Minneapolis, MN 55417, USA. manty001@maroon.tc.umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin ; Cell Membrane/metabolism ; Cells, Cultured ; Fluorescent Antibody Technique ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Injections, Spinal ; *N-Glycosyl Hydrolases ; Neurons/cytology/*metabolism ; Pain/physiopathology ; *Pain Management ; Pain Measurement ; Plant Proteins/metabolism/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/biosynthesis/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord/*cytology/metabolism ; Substance P/*metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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