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  • Articles  (82)
  • Signal Transduction  (82)
  • American Association for the Advancement of Science (AAAS)  (82)
  • American Association of Petroleum Geologists (AAPG)
  • Emerald
  • 1995-1999  (82)
  • 1997  (82)
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  • Articles  (82)
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  • American Association for the Advancement of Science (AAAS)  (82)
  • American Association of Petroleum Geologists (AAPG)
  • Emerald
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  • 1995-1999  (82)
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  • 1
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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
    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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  • 2
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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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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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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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  • 6
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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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  • 7
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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
    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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  • 8
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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
    Print ISSN: 0036-8075
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  • 9
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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
    Print ISSN: 0036-8075
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  • 10
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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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  • 11
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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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  • 12
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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)
    Details
    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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  • 13
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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)
    Details
    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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  • 14
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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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  • 15
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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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  • 16
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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)
    Details
    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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  • 17
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    PAS, present, and future: clues to the origins of circadian clocks (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 18
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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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  • 19
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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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  • 20
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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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  • 21
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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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  • 22
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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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  • 23
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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)
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    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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  • 24
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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)
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    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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt (1997)
    American Association for the Advancement of Science (AAAS)
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    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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    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)
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    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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    Calcium waves in retinal glial cells (1997)
    American Association for the Advancement of Science (AAAS)
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    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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  • 33
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    Nuclear export of NF-ATc enhanced by glycogen synthase kinase-3 (1997)
    American Association for the Advancement of Science (AAAS)
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    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)
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    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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    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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  • 36
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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)
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    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)
    Details
    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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    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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    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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  • 40
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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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  • 41
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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)
    Details
    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)
    Details
    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)
    Details
    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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  • 46
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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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    A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia (1997)
    American Association for the Advancement of Science (AAAS)
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    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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  • 54
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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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    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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    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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    Preserved acute pain and reduced neuropathic pain in mice lacking PKCgamma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    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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    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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    A G protein-coupled receptor phosphatase required for rhodopsin function (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Common and distinct roles of DFos and DJun during Drosophila development (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    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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    Antigen presentation by memory B cells: the sting is in the tail (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Effect of transmembrane and cytoplasmic domains of IgE on the IgE response (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
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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)
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    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
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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
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    Elementary calcium-release units induced by inositol trisphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: The extent to which inositol 1,4,5-trisphosphate (InsP3)-induced calcium signals are localized is a critical parameter for understanding the mechanism of effector activation. The spatial characteristics of InsP3-mediated calcium signals were determined by targeting a dextran-based calcium indicator to intracellular membranes through the in situ addition of a geranylgeranyl lipid group. Elementary calcium-release events observed with this indicator typically lasted less than 33 milliseconds, had diameters less than 2 micrometers, and were uncoupled from each other by the calcium buffer EGTA. Cellwide calcium transients are likely to result from synchronized triggering of such local release events, suggesting that calcium-dependent effector proteins could be selectively activated by localization near sites of local calcium release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horne, J H -- Meyer, T -- GM-51457/GM/NIGMS NIH HHS/ -- P01-HL-47053/HL/NHLBI NIH HHS/ -- R01-GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cytosol/metabolism ; Egtazic Acid/pharmacology ; Electroporation ; Fluorescent Dyes ; Inositol 1,4,5-Trisphosphate/*pharmacology ; Intracellular Membranes/*metabolism ; Kinetics ; Microscopy, Confocal ; Microscopy, Fluorescence ; Organic Chemicals ; Peptides/metabolism ; Rats ; Signal Transduction ; Tumor Cells, Cultured
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    Control of inflammation, cytokine expression, and germinal center formation by BCL-6 (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-04-25
    Description: The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted BCL-6 gene developed myocarditis and pulmonary vasculitis, had no germinal centers, and had increased expression of T helper cell type 2 cytokines. The BCL-6 DNA recognition motif resembled sites bound by the STAT (signal transducers and activators of transcription) transcription factors, which mediate cytokine signaling. BCL-6 could repress interleukin-4 (IL-4)-induced transcription when bound to a site recognized by the IL-4-responsive transcription factor Stat6. Thus, dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6-deficient mice and participate in lymphoid malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dent, A L -- Shaffer, A L -- Yu, X -- Allman, D -- Staudt, L M -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):589-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cells, Cultured ; Cytokines/*biosynthesis ; DNA-Binding Proteins/genetics/*physiology ; Ficoll/analogs & derivatives/immunology ; Germinal Center/*immunology ; Hemocyanin/immunology ; Immunoglobulins/biosynthesis ; Inflammation/*immunology/pathology ; Interferon-gamma/biosynthesis ; Interleukin-4/metabolism ; Interleukins/biosynthesis/metabolism ; Lymphocyte Activation ; Mice ; Myocarditis/immunology/pathology ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-6 ; Receptors, IgE/genetics ; STAT6 Transcription Factor ; Signal Transduction ; Spleen/immunology ; T-Lymphocytes/immunology ; Th2 Cells/immunology ; Trans-Activators/metabolism ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Trinitrobenzenes/immunology ; Vasculitis/immunology/pathology
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    Cocaine wreaks subtle damage on developing brains (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):38-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340757" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Attention/*drug effects ; Behavior/*drug effects ; Behavior, Animal/drug effects ; Brain/*drug effects/growth & development/physiology ; Child ; Child, Preschool ; Cocaine/*adverse effects ; Dopamine/metabolism ; Female ; Humans ; Infant ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Receptors, Dopamine D1/metabolism ; Serotonin/metabolism ; Signal Transduction
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    Bacterial interference caused by autoinducing peptide variants (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-06-27
    Description: The synthesis of virulence factors and other extracellular proteins by Staphylococcus aureus is globally controlled by the agr locus, which encodes a two-component signaling pathway whose activating ligand is an agr-encoded autoinducing peptide. The cognate peptides produced by some strains inhibit the expression of agr in other strains, and the amino acid sequences of peptide and receptor are markedly different between such strains, suggesting a hypervariability-generating mechanism. Cross-inhibition of gene expression represents a type of bacterial interference that could be correlated with the ability of one strain to exclude others from infection or colonization sites, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ji, G -- Beavis, R -- Novick, R P -- R01-AI30138/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2027-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute of Biomolecular Medicine, New York University Medical Center, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197262" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Antibiosis ; Bacterial Proteins/chemistry/*genetics/metabolism ; Cloning, Molecular ; Dimerization ; *Gene Expression Regulation, Bacterial ; Mass Spectrometry ; Molecular Sequence Data ; Peptides/chemistry/*genetics/metabolism ; Promoter Regions, Genetic ; Signal Transduction ; Staphylococcus aureus/*genetics/metabolism/pathogenicity ; *Trans-Activators ; Transcription Factors/chemistry/*genetics/metabolism ; Virulence
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    Putative cancer gene shows up in development instead (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):534-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Caenorhabditis elegans/genetics/growth & development ; Cell Adhesion Molecules/*metabolism ; Central Nervous System/abnormalities/embryology/*growth & development ; Chromosomes, Human, Pair 18 ; Colorectal Neoplasms/genetics ; *Genes, DCC ; Humans ; Mice ; Nerve Growth Factors/*metabolism ; Rats ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; *Tumor Suppressor Proteins
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    Bni1p, a yeast formin linking cdc42p and the actin cytoskeleton during polarized morphogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: The Saccharomyces cerevisiae BNI1 gene product (Bni1p) is a member of the formin family of proteins, which participate in cell polarization, cytokinesis, and vertebrate limb formation. During mating pheromone response, bni1 mutants showed defects both in polarized morphogenesis and in reorganization of the underlying actin cytoskeleton. In two-hybrid experiments, Bni1p formed complexes with the activated form of the Rho-related guanosine triphosphatase Cdc42p, with actin, and with two actin-associated proteins, profilin and Bud6p (Aip3p). Both Bni1p and Bud6p (like Cdc42p and actin) localized to the tips of mating projections. Bni1p may function as a Cdc42p target that links the pheromone response pathway to the actin cytoskeleton.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evangelista, M -- Blundell, K -- Longtine, M S -- Chow, C J -- Adames, N -- Pringle, J R -- Peter, M -- Boone, C -- GM31006/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):118-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082982" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Cell Cycle Proteins/*metabolism ; *Contractile Proteins ; Cytoskeleton/*metabolism ; Fungal Proteins/genetics/*metabolism ; GTP-Binding Proteins/*metabolism ; Microfilament Proteins/metabolism ; Morphogenesis ; Mutagenesis ; Profilins ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/*cytology/genetics/growth & development/*metabolism ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A broad-spectrum chemokine antagonist encoded by Kaposi's sarcoma-associated herpesvirus (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Kaposi's sarcoma-associated herpesvirus encodes a chemokine called vMIP-II. This protein displayed a broader spectrum of receptor activities than any mammalian chemokine as it bound with high affinity to a number of both CC and CXC chemokine receptors. Binding of vMIP-II, however, was not associated with the normal, rapid mobilization of calcium from intracellular stores; instead, it blocked calcium mobilization induced by endogenous chemokines. In freshly isolated human monocytes the virally encoded vMIP-II acted as a potent and efficient antagonist of chemotaxis induced by chemokines. Because vMIP-II could inhibit cell entry of human immunodeficiency virus (HIV) mediated through CCR3 and CCR5 as well as CXCR4, this protein may serve as a lead for development of broad-spectrum anti-HIV agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kledal, T N -- Rosenkilde, M M -- Coulin, F -- Simmons, G -- Johnsen, A H -- Alouani, S -- Power, C A -- Luttichau, H R -- Gerstoft, J -- Clapham, P R -- Clark-Lewis, I -- Wells, T N -- Schwartz, T W -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Molecular Pharmacology, Institute of Pharmacology, Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287217" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Cell Line ; Chemokine CCL5/antagonists & inhibitors ; Chemokines/*antagonists & inhibitors/chemistry/genetics/*metabolism/pharmacology ; Chemotaxis, Leukocyte ; HIV-1/physiology ; Herpesvirus 8, Human/*genetics ; Humans ; Molecular Sequence Data ; Monocytes/cytology ; Receptors, Cytokine/antagonists & inhibitors/*metabolism ; Receptors, HIV/antagonists & inhibitors/*metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction
    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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    Vascular system defects and impaired cell chemokinesis as a result of Galpha13 deficiency (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-24
    Description: Heterotrimeric GTP-binding proteins (G proteins) participate in cellular signaling and regulate a variety of physiological processes. Disruption of the gene encoding the G protein subunit alpha13 (Galpha13) in mice impaired the ability of endothelial cells to develop into an organized vascular system, resulting in intrauterine death. In addition, Galpha13 (-/-) embryonic fibroblasts showed greatly impaired migratory responses to thrombin. These results demonstrate that Galpha13 participates in the regulation of cell movement in response to specific ligands, as well as in developmental angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Offermanns, S -- Mancino, V -- Revel, J P -- Simon, M I -- AG 12288/AG/NIA NIH HHS/ -- GM 34236/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):533-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Bradykinin/pharmacology ; Cell Differentiation ; *Cell Movement/drug effects ; Cells, Cultured ; Embryo, Mammalian/metabolism ; Embryonic and Fetal Development ; Endothelium, Vascular/*cytology/embryology ; Female ; Fibronectins/pharmacology ; GTP-Binding Proteins/genetics/*physiology ; Gene Expression ; Gene Targeting ; Heterozygote ; Homozygote ; Lysophospholipids/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; *Neovascularization, Physiologic ; Signal Transduction ; Thrombin/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Role of transforming growth factor-beta in long-term synaptic facilitation in Aplysia (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-02-28
    Description: The role of transforming growth factor-beta (TGF-beta) in long-term synaptic facilitation was examined in isolated Aplysia ganglia. Treatment with TGF-beta1 induced long-term facilitation (24 and 48 hours), but not short-term (5 to 15 minutes) or intermediate-term (2 to 4 hours) facilitation. The long-term effects of TGF-beta1 were not additive with those of serotonin. Moreover, serotonin-induced facilitation was blocked by an inhibitor of TGF-beta. Thus, activation of TGF-beta may be part of the cascade of events underlying long-term sensitization, consistent with the hypothesis that signaling molecules that participate in development also have roles in adult neuronal plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, F -- Endo, S -- Cleary, L J -- Eskin, A -- Byrne, J H -- K05 MH-00649/MH/NIMH NIH HHS/ -- R01-NS-19895/NS/NINDS NIH HHS/ -- R01-NS-28462/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1318-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/*physiology ; Electric Stimulation ; Motor Neurons/physiology ; *Neuronal Plasticity ; Neurons, Afferent/physiology ; Protein-Serine-Threonine Kinases ; Receptors, Transforming Growth Factor beta/physiology ; Serotonin/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Transforming Growth Factor beta/*pharmacology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of cell cycle synchronization by decapentaplegic during Drosophila eye development (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: In the developing Drosophila eye, differentiation is coordinated with synchronized progression through the cell cycle. Signaling mediated by the transforming growth factor-beta-related gene decapentaplegic (dpp) was required for the synchronization of the cell cycle but not for cell fate specification. DPP may affect cell cycle synchronization by promoting cell cycle progression through the G2-M phases. This synchronization is critical for the precise assembly of the eye.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penton, A -- Selleck, S B -- Hoffmann, F M -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):203-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin Medical School, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; *Cell Cycle ; Cell Differentiation ; Cell Nucleus/ultrastructure ; Cyclins/metabolism ; Drosophila/*genetics/physiology ; *Drosophila Proteins ; Eye/cytology ; Female ; G1 Phase ; G2 Phase ; *Genes, Insect ; Insect Proteins/*genetics/physiology ; Male ; Membrane Glycoproteins/genetics/physiology ; Mitosis ; Mutation ; Photoreceptor Cells, Invertebrate/*cytology ; Proteoglycans/genetics/physiology ; Signal Transduction
    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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    Transformation of chicken cells by the gene encoding the catalytic subunit of PI 3-kinase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: The avian sarcoma virus 16 (ASV 16) is a retrovirus that induces hemangiosarcomas in chickens. Analysis of the ASV 16 genome revealed that it encodes an oncogene that is derived from the cellular gene for the catalytic subunit of phosphoinositide 3-kinase (PI 3-kinase). The gene is referred to as v-p3k, and like its cellular counterpart c-p3k, it is a potent transforming gene in cultured chicken embryo fibroblasts (CEFs). The products of the viral and cellular p3k genes have PI 3-kinase activity. CEFs transformed with either gene showed elevated levels of phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate and activation of Akt kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, H W -- Aoki, M -- Fruman, D -- Auger, K R -- Bellacosa, A -- Tsichlis, P N -- Cantley, L C -- Roberts, T M -- Vogt, P K -- CA 42564/CA/NCI NIH HHS/ -- GM 41890/GM/NIGMS NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1848-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Experimental Medicine, 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/9188528" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Avian Sarcoma Viruses/*genetics/physiology ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Cells, Cultured ; Chick Embryo ; Chickens ; Cloning, Molecular ; Enzyme Activation ; Genes, Viral ; Hemangiosarcoma/genetics/virology ; Molecular Sequence Data ; *Oncogenes ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/*genetics/metabolism ; Platelet-Derived Growth Factor/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Signal Transduction ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    STAT3 as an adapter to couple phosphatidylinositol 3-kinase to the IFNAR1 chain of the type I interferon receptor (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-30
    Description: STAT (signal transducers and activators of transcription) proteins undergo cytokine-dependent phosphorylation on serine and tyrosine. STAT3, a transcription factor for acute phase response genes, was found to act as an adapter molecule in signal transduction from the type I interferon receptor. STAT3 bound to a conserved sequence in the cytoplasmic tail of the IFNAR1 chain of the receptor and underwent interferon-dependent tyrosine phosphorylation. The p85 regulatory subunit of phosphatidylinositol 3-kinase, which activates a series of serine kinases, bound to phosphorylated STAT3 and subsequently underwent tyrosine phosphorylation. Thus, STAT3 acts as an adapter to couple another signaling pathway to the interferon receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeffer, L M -- Mullersman, J E -- Pfeffer, S R -- Murti, A -- Shi, W -- Yang, C H -- New York, N.Y. -- Science. 1997 May 30;276(5317):1418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162009" target="_blank"〉PubMed〈/a〉
    Keywords: Acute-Phase Proteins/*genetics ; Amino Acid Sequence ; Androstadienes/pharmacology ; Animals ; Binding Sites ; COS Cells ; Cell Line ; Cloning, Molecular ; Conserved Sequence ; DNA-Binding Proteins/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; Membrane Proteins ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & ; inhibitors/genetics/*metabolism ; Point Mutation ; Protein Binding ; Receptor, Interferon alpha-beta ; Receptors, Interferon/*metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/genetics/*metabolism ; Tyrosine/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Learning mechanisms: the case for CaM-KII (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lisman, J -- Malenka, R C -- Nicoll, R A -- Malinow, R -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2001-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254, USA. lisman@binah.cc.brandeis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Hippocampus/metabolism ; *Long-Term Potentiation ; Memory ; Mice ; Mice, Transgenic ; Phosphorylation ; Receptors, AMPA/*metabolism ; Signal Transduction ; Synapses/*metabolism ; *Synaptic Transmission ; Vision, Ocular
    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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    One molecule orchestrates amoebae (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235631" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/metabolism ; Animals ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Dictyostelium/cytology/genetics/*growth & development/metabolism ; Gene Expression Regulation ; Genes, Protozoan ; Mutation ; Signal Transduction
    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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