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  • Male  (1,030)
  • Cell Line  (538)
  • American Association for the Advancement of Science (AAAS)  (1,540)
  • American Chemical Society (ACS)
  • 1990-1994  (766)
  • 1980-1984  (774)
Collection
Keywords
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  • American Association for the Advancement of Science (AAAS)  (1,540)
  • American Chemical Society (ACS)
  • Springer  (2)
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Year
  • 1
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    CD26 antigen and HIV fusion? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patience, C -- McKnight, A -- Clapham, P R -- Boyd, M T -- Weiss, R A -- Schulz, T F -- G117/547/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 1994 May 20;264(5162):1159-60; author reply 1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909960" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*physiology ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Base Sequence ; Cats ; Cell Line ; Dipeptidyl Peptidase 4 ; HIV-1/*physiology ; Humans ; Mink ; Molecular Sequence Data
    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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    Microtubule severing by elongation factor 1 alpha (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: An activity that severs stable microtubules is thought to be involved in microtubule reorganization during the cell cycle. Here, a 48-kilodalton microtubule-severing protein was purified from Xenopus eggs and identified as translational elongation factor 1 alpha (EF-1 alpha). Bacterially expressed human EF-1 alpha also displayed microtubule-severing activity in vitro and, when microinjected into fibroblasts, induced rapid and transient fragmentation of cytoplasmic microtubule arrays. Thus, EF-1 alpha, an essential component of the eukaryotic translational apparatus, appears to have a second role as a regulator of cytoskeletal rearrangements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shiina, N -- Gotoh, Y -- Kubomura, N -- Iwamatsu, A -- Nishida, E -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Molecular Biology, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939665" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Humans ; Microtubules/drug effects/*metabolism ; Molecular Sequence Data ; Molecular Weight ; Oocytes ; Peptide Elongation Factor 1 ; Peptide Elongation Factors/chemistry/isolation & purification/*physiology ; Rats ; Recombinant Proteins/pharmacology ; Ribonucleoproteins/chemistry/isolation & purification/*physiology ; Sepharose/analogs & derivatives/metabolism ; Xenopus laevis
    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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  • 3
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    DNA loop repair by human cell extracts (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: An activity in human cell extracts is described that repairs DNA with loops of five or more unpaired bases. Repair is strand-specific and is directed by a nick located 5' or 3' to the loop. This repair is observed in a colorectal cancer cell line that is devoid of a wild-type hMLH1 gene and is deficient in repair of mismatches. However, a cell line with deletions in both hMSH2 alleles is deficient in repair of both loops and mismatches. Defects in loop repair may be relevant to the repetitive-sequence instability observed in cancers and other hereditary diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umar, A -- Boyer, J C -- Kunkel, T A -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):814-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973637" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Base Composition ; Base Sequence ; Carrier Proteins ; Cell Extracts ; Cell Line ; Colorectal Neoplasms/*genetics ; *DNA Repair ; DNA, Satellite/genetics/metabolism ; *DNA-Binding Proteins ; HeLa Cells ; Humans ; Molecular Sequence Data ; MutS Homolog 2 Protein ; Neoplasm Proteins/*genetics/physiology ; Nuclear Proteins ; Nucleic Acid Heteroduplexes/*metabolism ; Proto-Oncogene Proteins/*genetics/physiology ; Repetitive Sequences, Nucleic Acid ; Tumor Cells, Cultured
    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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    Suppression of Ras-induced transformation of NIH 3T3 cells by activated G alpha s (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: Conversion of external signals into proliferative responses may be mediated by interactions between signaling pathways that control cell proliferation. Interactions between G alpha s, the alpha subunit of the heterotrimeric guanine nucleotide binding protein that stimulates adenylyl cyclase, and Ras, an important element in growth factor signaling, were studied. Expression of activated G alpha s in NIH 3T3 cells increased intracellular concentrations of adenosine 3',5'-monophosphate (cAMP) and inhibited H-Ras-stimulated DNA synthesis and mitogen-activated protein kinase activity. Activated G alpha s and 8-Br-cAMP suppressed H-Ras-induced transformation of NIH 3T3 cells. Apparently, G alpha s inhibits proliferative signals from Ras by stimulating cAMP production and activating protein kinase A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- Iyengar, R -- CA-44998/CA/NCI NIH HHS/ -- DK-38761/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Mount Sinai School of Medicine, City University of New York, NY 10029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122111" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; GTP-Binding Proteins/genetics/*physiology ; *Genes, ras ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mutagenesis, Site-Directed ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Functional participation of the IL-2 receptor gamma chain in IL-7 receptor complexes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, M -- Takeshita, T -- Higuchi, M -- Nakamura, M -- Sudo, T -- Nishikawa, S -- Sugamura, K -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1453-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Female ; Genetic Linkage ; Interleukin-7/*metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin/*metabolism ; Receptors, Interleukin-2/genetics/immunology/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/*immunology ; X Chromosome
    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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  • 6
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    Thalamic abnormalities in schizophrenia visualized through magnetic resonance image averaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Schizophrenia is a complex illness characterized by multiple types of symptoms involving many aspects of cognition and emotion. Most efforts to identify its underlying neural substrates have focused on a strategy that relates a single symptom to a single brain region. An alternative hypothesis, that the variety of symptoms could be explained by a lesion in midline neural circuits mediating attention and information processing, is explored. Magnetic resonance images from patients and controls were transformed with a "bounding box" to produce an "average schizophrenic brain" and an "average normal brain." After image subtraction of the two averages, the areas of difference were displayed as an effect size map. Specific regional abnormalities were observed in the thalamus and adjacent white matter. An abnormality in the thalamus and related circuitry explains the diverse symptoms of schizophrenia parsimoniously because they could all result from a defect in filtering or gating sensory input, which is one of the primary functions of the thalamus in the human brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andreasen, N C -- Arndt, S -- Swayze, V 2nd -- Cizadlo, T -- Flaum, M -- O'Leary, D -- Ehrhardt, J C -- Yuh, W T -- MH31593/MH/NIMH NIH HHS/ -- MH40856/MH/NIMH NIH HHS/ -- MHCRC 43271/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):294-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mental Health Clinical Research Center, College of Medicine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939669" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/pathology ; Female ; Humans ; Image Processing, Computer-Assisted ; Magnetic Resonance Imaging/*methods ; Male ; Schizophrenia/*pathology ; Software ; Subtraction Technique ; Thalamus/*pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettit, D L -- Perlman, S -- Malinow, R -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1881-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Iowa, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997883" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Genetic Vectors ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Membrane Potentials ; Patch-Clamp Techniques ; Pyramidal Cells/enzymology/*physiology ; Rats ; Recombinant Proteins/metabolism ; Synaptic Transmission/drug effects/*physiology ; Transfection ; Vaccinia virus/genetics/physiology
    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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  • 8
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    Detection of endogenous malondialdehyde-deoxyguanosine adducts in human liver (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-09
    Description: Endogenous DNA adducts may contribute to the etiology of human genetic disease and cancer. One potential source of endogenous DNA adducts is lipid peroxidation, which generates mutagenic carbonyl compounds such as malondialdehyde. A sensitive mass spectrometric method permitted detection and quantitation of the major malondialdehyde-DNA adduct, a pyrimidopurinone derived from deoxyguanosine. DNA from disease-free human liver was found to contain 5400 adducts per cell, a frequency comparable to that of adducts formed by exogenous carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhary, A K -- Nokubo, M -- Reddy, G R -- Yeola, S N -- Morrow, J D -- Blair, I A -- Marnett, L J -- CA47479/CA/NCI NIH HHS/ -- ES00267/ES/NIEHS NIH HHS/ -- GM42056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1580-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A. B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt University School of Medicine, Nashville, TN 37232-0146.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079172" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Carbon Tetrachloride/toxicity ; DNA/*chemistry ; DNA Damage ; Deoxyguanosine/*analogs & derivatives/analysis/*metabolism ; Female ; Gas Chromatography-Mass Spectrometry ; Humans ; Lipid Peroxidation ; Liver/*chemistry ; Male ; Malondialdehyde/*metabolism ; Rats ; Rats, Sprague-Dawley
    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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  • 9
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    Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Representational difference analysis was used to isolate unique sequences present in more than 90 percent of Kaposi's sarcoma (KS) tissues obtained from patients with acquired immunodeficiency syndrome (AIDS). These sequences were not present in tissue DNA from non-AIDS patients, but were present in 15 percent of non-KS tissue DNA samples from AIDS patients. The sequences are homologous to, but distinct from, capsid and tegument protein genes of the Gammaherpesvirinae, herpesvirus saimiri and Epstein-Barr virus. These KS-associated herpesvirus-like (KSHV) sequences appear to define a new human herpesvirus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Y -- Cesarman, E -- Pessin, M S -- Lee, F -- Culpepper, J -- Knowles, D M -- Moore, P S -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1865-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997879" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; Amino Acid Sequence ; Base Composition ; Base Sequence ; Blotting, Southern ; Cloning, Molecular ; DNA, Viral/*analysis/chemistry/genetics ; Female ; Herpesviridae/*genetics ; Herpesvirus 2, Saimiriine/genetics ; Herpesvirus 4, Human/genetics ; Humans ; Male ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Open Reading Frames ; Polymerase Chain Reaction ; Retrospective Studies ; Sarcoma, Kaposi/etiology/*virology ; Sequence Homology, Amino Acid
    Print ISSN: 0036-8075
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  • 10
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    'Lucy,' crucial early human ancestor, finally gets a head (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shreeve, J -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):34-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ethiopia ; Female ; *Fossils ; History, Ancient ; *Hominidae ; Humans ; Male ; *Skull
    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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  • 11
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    Cooperative display and relatedness among males in a lek-mating bird (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: Long-tailed manakins mate in leks and cooperate in multiyear male-male partnerships. An alpha male is responsible for virtually all mating, whereas a beta male assists in the courtship displays. Such altruism by the beta male poses a problem for evolutionary theory because most theoretical treatments and empirical examples of cooperative behavior involve kin selection or reciprocity. Here it is shown that alpha and beta partners are not relatives and that reciprocity is not involved. Instead, direct, though long-delayed benefits to beta males are demonstrated, which include rare copulations, ascension to alpha status, and female lek fidelity. These benefits maintain this unusual form of male-male cooperation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, D B -- Potts, W K -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1030-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Archbold Biological Station, Lake Placid, FL 33852-2057.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973654" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Birds/genetics/*physiology ; *Cooperative Behavior ; Copulation ; Female ; Heterozygote ; Male ; Molecular Sequence Data ; Polymerase Chain Reaction ; *Sexual Behavior, Animal
    Print ISSN: 0036-8075
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  • 12
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    Finding 'sustainable' ways to prevent parasitic diseases (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolberg, R -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1859-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bedding and Linens ; Disease Vectors ; Dracunculiasis/prevention & control ; Female ; Fishes ; Humans ; Insect Control/*methods ; Malaria/prevention & control ; Male ; Parasitic Diseases/*prevention & control ; Pest Control, Biological/*methods ; Schistosomiasis/prevention & control ; World Health Organization
    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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  • 13
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    Insights into reproduction (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischman, J -- Ray, L B -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1459.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Contraception ; Female ; Humans ; Male ; *Reproduction/genetics/physiology ; Sex Differentiation
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  • 14
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    Inhibition of NF-kappa B by sodium salicylate and aspirin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: The transcription factor nuclear factor-kappa B (NF-kappa B) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kopp, E -- Ghosh, S -- R01 AI 33443-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):956-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06536.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/*pharmacology ; Cell Line ; Enhancer Elements, Genetic ; Gene Expression/drug effects ; Genes, Reporter ; HIV Long Terminal Repeat ; HIV-1/genetics ; Humans ; Immunoglobulin kappa-Chains/genetics ; Lipopolysaccharides/pharmacology ; Mice ; NF-kappa B/*antagonists & inhibitors/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Biosynthesis/drug effects ; Proto-Oncogene Proteins/metabolism ; Sodium Salicylate/*pharmacology ; T-Lymphocytes/metabolism ; Transcription Factor RelB ; *Transcription Factors ; 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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  • 15
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    Genetic mapping of quantitative trait loci for growth and fatness in pigs (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: The European wild boar was crossed with the domesticated Large White pig to genetically dissect phenotypic differences between these populations for growth and fat deposition. The most important effects were clustered on chromosome 4, with a single region accounting for a large part of the breed difference in growth rate, fatness, and length of the small intestine. The study is an advance in genome analyses and documents the usefulness of crosses between divergent outbred populations for the detection and characterization of quantitative trait loci. The genetic mapping of a major locus for fat deposition in the pig could have implications for understanding human obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andersson, L -- Haley, C S -- Ellegren, H -- Knott, S A -- Johansson, M -- Andersson, K -- Andersson-Eklund, L -- Edfors-Lilja, I -- Fredholm, M -- Hansson, I -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1771-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, Uppsala.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134840" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*anatomy & histology ; Animals ; *Chromosome Mapping ; Crosses, Genetic ; Disease Models, Animal ; Female ; *Genes ; Genetic Markers ; Humans ; Intestine, Small/anatomy & histology ; Likelihood Functions ; Male ; Obesity/genetics ; Phenotype ; Swine/anatomy & histology/*genetics/growth & development
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Receptor and ligand domains for invasion of erythrocytes by Plasmodium falciparum (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: A 175-kilodalton erythrocyte binding protein, EBA-175, of the parasite Plasmodium falciparum mediates the invasion of erythrocytes. The erythrocyte receptor for EBA-175 is dependent on sialic acid. The domain of EBA-175 that binds erythrocytes was identified as region II with the use of truncated portions of EBA-175 expressed on COS cells. Region II, which contains a cysteine-rich motif, and native EBA-175 bind specifically to glycophorin A, but not to glycophorin B, on the erythrocyte membrane. Erythrocyte recognition of EBA-175 requires both sialic acid and the peptide backbone of glycophorin A. The identification of both the receptor and ligand domains may suggest rational designs for receptor blockade and vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sim, B K -- Chitnis, C E -- Wasniowska, K -- Hadley, T J -- Miller, L H -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1941-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Malaria Research, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Protozoan ; Base Sequence ; Binding Sites ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Erythrocytes/metabolism/*parasitology ; Glycopeptides/chemistry/metabolism ; Glycophorin/chemistry/*metabolism ; Molecular Sequence Data ; Plasmodium falciparum/*metabolism ; Protozoan Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sialic Acids/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Insights from the study of animals lacking functional estrogen receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Estrogen hormones produce physiological actions within a variety of target sites in the body and during development by activating a specific receptor protein. Hormone responsiveness for the estrogen receptor protein was investigated at different stages of development with the use of gene knockout techniques because no natural genetic mutants have been described. A mutant mouse line without a functional estrogen receptor was created and is being used to assess estrogen responsiveness. Both sexes of these mutant animals are infertile and show a variety of phenotypic changes, some of which are associated with the gonads, mammary glands, reproductive tracts, and skeletal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korach, K S -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1524-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estrogens/*physiology ; Female ; Heterozygote ; Homozygote ; Humans ; Infertility, Female/etiology ; Infertility, Male/etiology ; Male ; Mice ; Mice, Knockout ; Mutation ; Phenotype ; Receptors, Estrogen/genetics/*physiology ; Signal Transduction
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  • 18
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    Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-25
    Description: Fas is an apoptosis-signaling receptor molecule on the surface of a number of cell types. Molecular cloning and nucleotide sequence analysis revealed a human Fas messenger RNA variant capable of encoding a soluble Fas molecule lacking the transmembrane domain because of the deletion of an exon encoding this region. The expression of soluble Fas was confirmed by flow cytometry and immunocytochemical analysis. Supernatants from cells transfected with the variant messenger RNA blocked apoptosis induced by the antibody to Fas. Levels of soluble Fas were elevated in patients with systemic lupus erythematosus, and mice injected with soluble Fas displayed autoimmune features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, J -- Zhou, T -- Liu, C -- Shapiro, J P -- Brauer, M J -- Kiefer, M C -- Barr, P J -- Mountz, J D -- P01 AR03555/AR/NIAMS NIH HHS/ -- P50 AI23694/AI/NIAID NIH HHS/ -- P60 AR20614/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1759-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Alabama at Birmingham.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7510905" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies/immunology ; Antigens, CD95 ; Antigens, Surface/chemistry/genetics/immunology/*physiology ; *Apoptosis ; Arthritis, Rheumatoid/blood ; Base Sequence ; Cell Line ; Cell Membrane/chemistry ; Humans ; Lupus Erythematosus, Systemic/blood ; Mice ; Molecular Sequence Data ; RNA, Messenger/genetics ; Solubility ; T-Lymphocyte Subsets/immunology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Effect of the nigrostriatal dopamine system on acquired neural responses in the striatum of behaving monkeys (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-15
    Description: Dysfunction of the nigrostriatal dopamine system results in marked disorders of movement such as occur in Parkinson's disease. Functions of this dopamine-containing projection system were examined in monkeys trained in a classical conditioning task, and the effects of striatal dopamine depletion were tested. Unilateral dopamine loss substantially reduced the acquired sensory responsiveness of striatal neurons monitored electrophysiologically. This effect was ipsilateral and selective, and could be reversed by apomorphine. These results suggest that the primate nigrostriatal system modulates expression of neuronal response plasticity in the striatum during sensorimotor learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aosaki, T -- Graybiel, A M -- Kimura, M -- R01 NS25529/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):412-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023166" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology ; Action Potentials/drug effects ; Animals ; Apomorphine/pharmacology ; *Behavior, Animal/drug effects ; *Conditioning, Classical ; Corpus Striatum/cytology/*physiology ; Dopamine/*physiology ; Haloperidol/pharmacology ; Macaca ; Male ; Neuronal Plasticity ; Neurons/drug effects/*physiology ; Substantia Nigra/cytology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Mediation of c-Myc-induced apoptosis by p53 (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-09-30
    Description: The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The same characteristics have been described for the tumor suppressor gene p53, the most commonly mutated gene in human cancer. In quiescent mouse fibroblasts expressing wild-type p53 protein, activation of c-Myc was found to induce apoptosis and cell cycle reentry, preceded by stabilization of p53. In contrast, in quiescent p53-null fibroblasts, activation of c-Myc induced cell cycle reentry but not apoptosis. These results suggest that p53 mediates apoptosis as a safeguard mechanism to prevent cell proliferation induced by oncogene activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hermeking, H -- Eick, D -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Molekularbiologie und Tumorgenetik Forschungszentrum fur Umwelt und Gesundheit, GSF, Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Apoptosis ; Cell Line ; Estradiol/pharmacology ; G1 Phase ; Gene Expression Regulation ; Genes, myc ; Genes, p53 ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism ; Tamoxifen/analogs & derivatives/pharmacology ; Transfection ; Tumor Suppressor Protein p53/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    SIDS paper triggers a murder charge (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinholster, G -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):197-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146647" target="_blank"〉PubMed〈/a〉
    Keywords: Apnea/*complications/history ; Female ; *Forensic Medicine ; History, 20th Century ; Humans ; Infant ; *Infanticide ; Male ; *Publishing/history ; Sudden Infant Death/*etiology
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  • 22
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    Mutagenesis and mapping of a mouse gene, Clock, essential for circadian behavior (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-04-29
    Description: In a search for genes that regulate circadian rhythms in mammals, the progeny of mice treated with N-ethyl-N-nitrosourea (ENU) were screened for circadian clock mutations. A semidominant mutation, Clock, that lengthens circadian period and abolishes persistence of rhythmicity was identified. Clock segregated as a single gene that mapped to the midportion of mouse chromosome 5, a region syntenic to human chromosome 4. The power of ENU mutagenesis combined with the ability to clone murine genes by map position provides a generally applicable approach to study complex behavior in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" 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/PMC3839659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitaterna, M H -- King, D P -- Chang, A M -- Kornhauser, J M -- Lowrey, P L -- McDonald, J D -- Dove, W F -- Pinto, L H -- Turek, F W -- Takahashi, J S -- P30-CA07175/CA/NCI NIH HHS/ -- R01-DK40493/DK/NIDDK NIH HHS/ -- T32 NS071040/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):719-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Circadian Rhythm/*genetics ; Ethylnitrosourea ; Female ; *Genes ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; *Mutagenesis ; Phenotype
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  • 23
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    Promoter-selective transcriptional defect in cell cycle mutant ts13 rescued by hTAFII250 (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-11
    Description: The TAFII250 subunit of the human transcription factor IID (TFIID) rescues the temperature-sensitive hamster cell line ts13 and overcomes a G1 arrest. Investigation of the transcriptional properties of ts13 nuclear extracts in vitro showed that activation by the site-specific regulators Sp1 and Gal4VP16 is temperature sensitive in ts13 extracts, whereas basal transcription remains unaffected. This transcriptional defect can be rescued by purified human TFIID or by expression of wild-type TAFII250 in ts13 cells. Expression from the cyclin A but not c-fos promoter is temperature sensitive in these mutant cells. Thus, the mutation in TAFII250 appears to have gene-specific effects that may lead to the ts13 cell cycle phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, E H -- Tjian, R -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):811-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cyclins/genetics ; DNA-Binding Proteins/*genetics/physiology ; Fungal Proteins/physiology ; *G1 Phase ; Genes, fos ; Genetic Complementation Test ; Genetic Vectors ; Histone Acetyltransferases ; Humans ; Mutation ; Nuclear Proteins/*genetics/physiology ; *Promoter Regions, Genetic ; Sp1 Transcription Factor/physiology ; *TATA-Binding Protein Associated Factors ; Temperature ; Trans-Activators/physiology ; Transcription Factor TFIID ; Transcription Factors/pharmacology ; *Transcription, Genetic ; Transfection
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  • 24
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    A genetic linkage map for the zebrafish (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-04-29
    Description: To facilitate molecular genetic analysis of vertebrate development, haploid genetics was used to construct a recombination map for the zebrafish Danio (Brachydanio) rerio. The map consists of 401 random amplified polymorphic DNAs (RAPDs) and 13 simple sequence repeats spaced at an average interval of 5.8 centimorgans. Strategies that exploit the advantages of haploid genetics and RAPD markers were developed that quickly mapped lethal and visible mutations and that placed cloned genes on the map. This map is useful for the position-based cloning of mutant genes, the characterization of chromosome rearrangements, and the investigation of evolution in vertebrate genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Postlethwait, J H -- Johnson, S L -- Midson, C N -- Talbot, W S -- Gates, M -- Ballinger, E W -- Africa, D -- Andrews, R -- Carl, T -- Eisen, J S -- 1RO1AI26734/AI/NIAID NIH HHS/ -- HD07470/HD/NICHD NIH HHS/ -- NS23915/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):699-703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurosciences, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Cloning, Molecular ; Female ; Genetic Markers ; Genotype ; Male ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid ; Software ; Zebrafish/*genetics
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  • 25
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    Transgenic X. laevis embryos from eggs transplanted with nuclei of transfected cultured cells (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-10-28
    Description: Transgenic Xenopus laevis embryos were produced by transplantation of transfected cultured cell nuclei into unfertilized eggs. A Xenopus cell line, X-C, was stably transfected with plasmids containing a hygromycin-resistance gene and genes for either beta-galactosidase with a heat shock promoter or chloramphenicol acetyltransferase (CAT) with a muscle-specific actin promoter. Nuclei transplanted from these cells into unfertilized eggs directed development of embryos containing stably integrated copies of the plasmids in each cell. Transgenic embryos showed somite-specific expression of CAT and uniform expression of beta-galactosidase. Transgenic embryos produced by nuclear transplantation should be useful for testing the function of cloned genes in amphibian development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kroll, K L -- Gerhart, J C -- GM07232/GM/NIGMS NIH HHS/ -- GM19363/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):650-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Line ; Cell Nucleus/genetics/physiology ; Chloramphenicol O-Acetyltransferase/genetics ; *Cinnamates ; Drug Resistance ; Embryo, Nonmammalian/*physiology ; *Gene Expression ; Genes, Reporter ; Hygromycin B/analogs & derivatives/pharmacology ; *Nuclear Transfer Techniques ; Ovum/physiology ; Plasmids ; Promoter Regions, Genetic ; *Transfection ; Xenopus laevis ; beta-Galactosidase/genetics
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  • 26
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    Identification of the ron gene product as the receptor for the human macrophage stimulating protein (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-10-07
    Description: Macrophage-stimulating protein (MSP) is a member of the hepatocyte growth factor-scatter factor (HGF-SF) family. Labeled MSP bound to Madin-Darby canine kidney (MDCK) cells transfected with complementary DNA encoding Ron, a cell membrane protein tyrosine kinase. Cross-linking of 125I-labeled MSP to transfected cells (MDCK-RE7 cells) and immunoprecipitation by antibodies to Ron revealed a 220-kilodalton complex, a size consistent with that of MSP (80 kilodaltons) cross-linked to the beta chain of Ron (150 kilodaltons). The binding of 125I-labeled MSP to MDCK-RE7 cells was inhibited by unlabeled MSP, but not by HGF-SF. MSP caused phosphorylation of the beta chain of Ron and induced migration of MDCK-RE7 cells. These results establish the ron gene product as a specific cell-surface receptor for MSP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, M H -- Ronsin, C -- Gesnel, M C -- Coupey, L -- Skeel, A -- Leonard, E J -- Breathnach, R -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):117-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunopathology Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Binding, Competitive ; Cell Line ; Cell Movement/drug effects ; Cross-Linking Reagents ; Dogs ; Growth Substances/*metabolism/pharmacology ; Hepatocyte Growth Factor/metabolism ; Humans ; Phosphorylation ; Plasminogen/metabolism ; *Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Transfection
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  • 27
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    Is a new virus the cause of KS? (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1803-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997874" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; DNA, Viral/*analysis ; Herpesviridae/*genetics/isolation & purification ; Homosexuality, Male ; Humans ; Male ; Sarcoma, Kaposi/etiology/*virology
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  • 28
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    Outcomes research (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wennberg, J E -- Barry, M J -- New York, N.Y. -- Science. 1994 May 6;264(5160):758-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7513442" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Male ; *Outcome Assessment (Health Care) ; Prostatectomy ; Prostatic Hyperplasia/surgery ; Randomized Controlled Trials as Topic ; United States ; United States Agency for Healthcare Research and Quality
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  • 29
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    Binding of 14-3-3 proteins to the protein kinase Raf and effects on its activation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: To identify proteins that may participate in the activation of the protein kinase Raf, proteins that interact with Raf were selected in a two-hybrid screen. Two members of the 14-3-3 protein family were isolated that interacted with both the amino terminal regulatory regions of Raf and the kinase domain of Raf, but did not compete with the guanine nucleotide-binding protein Ras for binding to Raf. 14-3-3 proteins associated with Raf in mammalian cells and accompanied Raf to the membrane in the presence of activated Ras. In yeast cells expressing Raf and MEK, mammalian 14-3-3 beta or 14-3-3 zeta activated Raf to a similar extent as did expression of Ras. Therefore, 14-3-3 proteins may participate in or be required for the regulation of Raf function. These findings suggest a role for 14-3-3 proteins in Raf-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, E -- Symons, M -- Macdonald, S G -- McCormick, F -- Ruggieri, R -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1713-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, Richmond, CA 94806-5206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085158" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/enzymology ; Cytosol/enzymology ; Enzyme Activation ; GTP-Binding Proteins/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1 ; *Mitogen-Activated Protein Kinase Kinases ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-raf ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development ; Signal Transduction ; *Tyrosine 3-Monooxygenase ; Zinc Fingers
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    Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: The proposal that nitric oxide (NO) or its reactant products mediate toxicity in brain remains controversial in part because of the use of nonselective agents that block NO formation in neuronal, glial, and vascular compartments. In mutant mice deficient in neuronal NO synthase (NOS) activity, infarct volumes decreased significantly 24 and 72 hours after middle cerebral artery occlusion, and the neurological deficits were less than those in normal mice. This result could not be accounted for by differences in blood flow or vascular anatomy. However, infarct size in the mutant became larger after endothelial NOS inhibition by nitro-L-arginine administration. Hence, neuronal NO production appears to exacerbate acute ischemic injury, whereas vascular NO protects after middle cerebral artery occlusion. The data emphasize the importance of developing selective inhibitors of the neuronal isoform.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Z -- Huang, P L -- Panahian, N -- Dalkara, T -- Fishman, M C -- Moskowitz, M A -- NS10828/NS/NINDS NIH HHS/ -- NS2636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1883-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stroke Research Laboratory, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522345" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/deficiency/*metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Brain/enzymology/*metabolism ; Brain Ischemia/complications/*metabolism ; Cerebral Infarction/*etiology ; Cerebrovascular Circulation ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Neurons/*enzymology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine
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    Diet and health: what should we eat? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-22
    Description: Many recent studies have implicated dietary factors in the cause and prevention of important diseases, including cancer, coronary heart disease, birth defects, and cataracts. There is strong evidence that vegetables and fruits protect against these diseases; however, the active constituents are incompletely identified. Whether fat per se is a major cause of disease is a question still under debate, although saturated and partially hydrogenated fats probably increase the risk of coronary heart disease. One clear conclusion from existing epidemiologic evidence is that many individuals in the United States have suboptimal diets and that the potential for disease prevention by improved nutrition is substantial.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willett, W C -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):532-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nutrition, Harvard School of Public Health, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8160011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coronary Disease/etiology/prevention & control ; Dairy Products ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats/administration & dosage ; Dietary Proteins/administration & dosage ; Female ; Fruit ; Humans ; Male ; Neoplasms/etiology/prevention & control ; *Nutritional Physiological Phenomena ; *Preventive Medicine ; United States ; Vegetables
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    Inhibition of hepatic chylomicron remnant uptake by gene transfer of a receptor antagonist (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The low density lipoprotein receptor-related protein (LRP) has been proposed to mediate in concert with the LDL receptor (LDLR) the uptake of dietary lipoproteins into the hepatocytes. This hypothesis was tested by transient inactivation of LRP in vivo. Receptor-associated protein (RAP), a dominant negative regulator of LRP function, was transferred by an adenoviral vector to the livers of mice lacking LDLR (LDLR-/-). The inactivation of LRP by RAP was associated with a marked accumulation of chylomicron remnants in LDLR-/- mice and to a lesser degree in normal mice, suggesting that both LDLR and LRP are involved in remnant clearance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willnow, T E -- Sheng, Z -- Ishibashi, S -- Herz, J -- HL20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7515194" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apolipoprotein B-48 ; Apolipoproteins B/*metabolism ; Carrier Proteins/genetics/*physiology ; Cholesterol/blood ; Chylomicrons/blood/*metabolism ; Gene Transfer Techniques ; Genetic Vectors ; Glycoproteins/genetics/*physiology ; LDL-Receptor Related Protein-Associated Protein ; Liver/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-1 ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Immunologic/antagonists & inhibitors/*metabolism ; Receptors, LDL/metabolism ; Triglycerides/blood ; alpha-Macroglobulins/metabolism
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    Model programs take aim at HIV rates in Indonesia (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, J E -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):24-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140414" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/epidemiology/*prevention & control ; Female ; Government Agencies ; Health Education ; Health Knowledge, Attitudes, Practice ; *Health Promotion ; Humans ; Indonesia/epidemiology ; Male ; United States ; World Health Organization
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    Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reuther, G W -- Fu, H -- Cripe, L D -- Collier, R J -- Pendergast, A M -- CA61033/CA/NCI NIH HHS/ -- DK01965/DK/NIDDK NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939633" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*metabolism ; Humans ; Mice ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcr ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Tyrosine 3-Monooxygenase
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    Targeting of G alpha i2 to the Golgi by alternative spliced carboxyl-terminal region (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: Heterotrimeric guanosine triphosphate (GTP)-binding proteins (G proteins) may participate in membrane traffic events. A complementary DNA (cDNA) was isolated from a mouse pituitary cDNA library that corresponded to an alternatively spliced form of the gene encoding the G protein alpha subunit G alpha i2. The cDNA was identical to that encoding G alpha i2 except that the region encoding for the carboxyl-terminal 24 amino acids was replaced by a longer region encoding 35 amino acids that have no sequence similarity with G alpha i2 or other members of the G protein family. This alternative spliced product and the corresponding protein (sGi2) were present in several tissues. Specific antibodies revealed that sGi2 was localized in the Golgi apparatus, suggesting a role in membrane transport. Thus, alternative splicing may generate from a single gene two G protein alpha subunits with differential cellular localization and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montmayeur, J P -- Borrelli, E -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):95-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes, CNRS, INSERM U184, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272874" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Coatomer Protein ; DNA, Complementary/genetics ; GTP-Binding Protein alpha Subunit, Gi2 ; *GTP-Binding Protein alpha Subunits, Gi-Go ; GTP-Binding Proteins/analysis/chemistry/genetics/*metabolism ; Golgi Apparatus/chemistry/*metabolism ; Mice ; Microtubule-Associated Proteins/analysis ; Molecular Sequence Data ; Oncogene Proteins/analysis/chemistry/genetics/*metabolism ; *Proto-Oncogene Proteins
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    Degeneration of a nonrecombining chromosome (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: Comparative studies suggest that sex chromosomes begin as ordinary autosomes that happen to carry a major sex determining locus. Over evolutionary time the Y chromosome is selected to stop recombining with the X chromosome, perhaps in response to accumulation of alleles beneficial to the heterogametic but harmful to the homogametic sex. Population genetic theory predicts that a nonrecombining Y chromosome should degenerate. Here this prediction is tested by application of specific selection pressures to Drosophila melanogaster populations. Results demonstrate the decay of a nonrecombining, nascent Y chromosome and the capacity for recombination to ameliorate such decay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, W R -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):230-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Santa Cruz 95064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284674" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Drosophila melanogaster/*genetics/physiology ; Female ; Haplotypes ; Male ; Mutation ; *Recombination, Genetic ; *Y Chromosome
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    Risk from low-dose exposures (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monro, A M -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/*statistics & numerical data ; Carcinogens/*administration & dosage/toxicity ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Mice ; Mutagenicity Tests ; Neoplasms/*chemically induced ; Rats ; Risk Assessment
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    Localization of a breast cancer susceptibility gene, BRCA2, to chromosome 13q12-13 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: A small proportion of breast cancer, in particular those cases arising at a young age, is due to the inheritance of dominant susceptibility genes conferring a high risk of the disease. A genomic linkage search was performed with 15 high-risk breast cancer families that were unlinked to the BRCA1 locus on chromosome 17q21. This analysis localized a second breast cancer susceptibility locus, BRCA2, to a 6-centimorgan interval on chromosome 13q12-13. Preliminary evidence suggests that BRCA2 confers a high risk of breast cancer but, unlike BRCA1, does not confer a substantially elevated risk of ovarian cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wooster, R -- Neuhausen, S L -- Mangion, J -- Quirk, Y -- Ford, D -- Collins, N -- Nguyen, K -- Seal, S -- Tran, T -- Averill, D -- CA-48711/CA/NCI NIH HHS/ -- CN-05222/CN/NCI NIH HHS/ -- HG-00571/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2088-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Carcinogenesis, Institute of Cancer Research, Sutton, Surrey, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091231" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Female ; Genes, Retinoblastoma ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Lod Score ; Male ; Ovarian Neoplasms/genetics ; Pedigree ; Phenotype
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  • 39
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    The Drosophila saxophone gene: a serine-threonine kinase receptor of the TGF-beta superfamily (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: The Drosophila decapentaplegic (dpp) gene encodes a transforming growth factor-beta (TGF-beta)-like protein that plays a key role in several aspects of development. Transduction of the DPP signal was investigated by cloning of serine-threonine kinase transmembrane receptors from Drosophila because this type of receptor is specific for the TGF-beta-like ligands. Here evidence is provided demonstrating that the Drosophila saxophone (sax) gene, a previously identified female sterile locus, encodes a TGF-beta-like type I receptor. Embryos from sax mothers and dpp embryos exhibit similar mutant phenotypes during early gastrulation, and these two loci exhibit genetic interactions, which suggest that they are utilized in the same pathway. These data suggest that sax encodes a receptor for dpp.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, T -- Finelli, A L -- Padgett, R W -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1756-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Waksman Institute, Rutgers University, Piscataway, NJ 08855-0759.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134837" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; Drosophila/embryology/*genetics/metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Female ; *Genes, Insect ; Insect Hormones/genetics/*metabolism ; Male ; Molecular Sequence Data ; Mutation ; Protein-Serine-Threonine Kinases/chemistry/*genetics/metabolism ; Receptors, Transforming Growth Factor beta/chemistry/*genetics/metabolism ; Signal Transduction ; Transforming Growth Factor beta/genetics/*metabolism
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  • 40
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    Regulation of MHC class I transport by the molecular chaperone, calnexin (p88, IP90) (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-21
    Description: Assembled class I histocompatibility molecules, consisting of heavy chain, beta 2-microglobulin, and peptide ligand, are transported rapidly to the cell surface. In contrast, the intracellular transport of free heavy chains or peptide-deficient heavy chain-beta 2-microglobulin heterodimers is impaired. A 90-kilodalton membrane-bound chaperone of the endoplasmic reticulum (ER), termed calnexin, associates quantitatively with newly synthesized class I heavy chains, but the functions of calnexin in this interaction are unknown. Class I subunits were expressed alone or in combination with calnexin in Drosophila melanogaster cells. Calnexin retarded the intracellular transport of both peptide-deficient heavy chain-beta 2-microglobulin heterodimers and free heavy chains. Calnexin also impeded the rapid intracellular degradation of free heavy chains. The ability of calnexin to protect and retain class I assembly intermediates is likely to contribute to the efficient intracellular formation of class I-peptide complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, M R -- Cohen-Doyle, M F -- Peterson, P A -- Williams, D B -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):384-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278813" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Calcium-Binding Proteins/*metabolism ; Calnexin ; Cell Line ; Drosophila melanogaster ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; Histocompatibility Antigens Class I/*metabolism ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Temperature ; Transfection ; beta 2-Microglobulin/*metabolism
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  • 41
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    Sequential interactions of the TCR with two distinct cytoplasmic tyrosine kinases (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: The T cell antigen receptor (TCR) initiates signals by interacting with cytoplasmic protein tyrosine kinases (PTKs) through a 17-residue sequence motif [called the antigen recognition activation motif (ARAM)] that is contained in the TCR zeta and CD3 chains. TCR stimulation induces the tyrosine phosphorylation of several cellular substrates, including the ARAMs. Lck kinase activity is required for phosphorylation of two conserved tyrosine residues in an ARAM. This phosphorylation leads to the recruitment of a second cytoplasmic PTK, ZAP-70, through both of the ZAP-70 Src homology 2 domains and its phosphorylation. Thus, TCR signal transduction is initiated by the sequential interaction of two PTKs with TCR ARAMs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashima, M -- Irving, B A -- van Oers, N S -- Chan, A C -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1136-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509083" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD8/metabolism ; Cell Line ; Cytoplasm/enzymology ; Haplorhini ; Humans ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism ; ZAP-70 Protein-Tyrosine Kinase
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    New tool for predicting AIDS onset? (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Feb 4;263(5147):606.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303266" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; HIV/*physiology ; HIV Seropositivity/*microbiology ; Humans ; Male ; RNA, Messenger/*blood ; RNA, Viral/*blood ; Virus Replication
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    Genetics of a pheromonal difference contributing to reproductive isolation in Drosophila (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: Although sexual isolation is one of the most important causes of speciation, its genetic basis is largely unknown. Here evidence is presented that suggests that sexual isolation between two closely related species of Drosophila is largely caused by differences in female cuticular hydrocarbons. This difference maps to only one of the three major chromosomes, implying that reproductive isolation might have a fairly simple genetic basis. The effect of the hydrocarbons on courtship may help explain the ubiquitous asymmetry of sexual isolation between many pairs of Drosophila species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coyne, J A -- Crittenden, A P -- Mah, K -- GM 38462/GM/NIGMS NIH HHS/ -- GM 50355/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1461-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolution, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Chromosome Mapping ; Crosses, Genetic ; Drosophila/*genetics/physiology ; Female ; *Genes, Insect ; Genetic Markers ; Male ; Pheromones/analysis/*genetics/physiology ; Reproduction ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 44
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    Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: Rasmussen's encephalitis is a progressive childhood disease of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain. During efforts to raise antibodies to recombinant glutamate receptors (GluRs), behaviors typical of seizures and histopathologic features mimicking Rasmussen's encephalitis were found in two rabbits immunized with GluR3 protein. A correlation was found between the presence of Rasmussen's encephalitis and serum antibodies to GluR3 detected by protein immunoblot analysis and by immunoreactivity to transfected cells expressing GluR3. Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function. Thus, GluR3 is an autoantigen in Rasmussen's encephalitis, and an autoimmune process may underlie this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, S W -- Andrews, P I -- Gahring, L C -- Whisenand, T -- Cauley, K -- Crain, B -- Hughes, T E -- Heinemann, S F -- McNamara, J O -- NS17771/NS/NINDS NIH HHS/ -- NS28709/NS/NINDS NIH HHS/ -- NS30990R29/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):648-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salt Lake City Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center, UT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Autoantibodies/blood/*immunology ; Brain/pathology ; Cell Line ; Child ; Disease Models, Animal ; Encephalitis/complications/*immunology/pathology/therapy ; Female ; Humans ; Male ; Plasma Exchange ; Rabbits ; Receptors, Glutamate/*immunology ; Recombinant Fusion Proteins/immunology ; Seizures/etiology/immunology
    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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  • 45
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    Transcriptional activation modulated by homopolymeric glutamine and proline stretches (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: Many transcription factors contain proline- or glutamine-rich activation domains. Here it is shown that simple homopolymeric stretches of these amino acids can activate transcription when fused to the DNA binding domain of GAL4 factor. In vitro, activity increased with polymer length, whereas in cell transfection assays maximal activity was achieved by 10 to 30 glutamines or about 10 prolines. Similar results were obtained when glutamine stretches were placed within a [GAL4]-VP16 chimeric protein. Because these stretches are encoded by rapidly evolving triplet repeats (microsatellites), they may be the main cause for modulation of transcription factor activity and thus result in subtle or overt genomic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerber, H P -- Seipel, K -- Georgiev, O -- Hofferer, M -- Hug, M -- Rusconi, S -- Schaffner, W -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):808-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molekularbiologie II der Universitat Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303297" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Glutamine/*chemistry/pharmacology ; HeLa Cells ; Humans ; Molecular Sequence Data ; Peptides/*chemistry/pharmacology ; Recombinant Fusion Proteins/pharmacology ; Repetitive Sequences, Nucleic Acid ; Transcription Factors/*chemistry/pharmacology ; *Transcriptional Activation ; Transfection
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  • 46
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    The thermal grill illusion: unmasking the burn of cold pain (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: In Thunberg's thermal grill illusion, first demonstrated in 1896, a sensation of strong, often painful heat is elicited by touching interlaced warm and cool bars to the skin. Neurophysiological recordings from two classes of ascending spinothalamic tract neurons that are sensitive to innocuous or noxious cold showed differential responses to the grill. On the basis of these results, a simple model of central disinhibition, or unmasking, predicted a quantitative correspondence between grill-evoked pain and cold-evoked pain, which was verified psychophysically. This integration of pain and temperature can explain the thermal grill illusion and the burning sensation of cold pain and may also provide a basis for the cold-evoked, burning pain of the classic thalamic pain syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Craig, A D -- Bushnell, M C -- DA07402/DA/NIDA NIH HHS/ -- NS25616/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):252-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Barrow Neurological Institute, Phoenix, AZ 85013.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023144" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cats ; *Cold Temperature ; Female ; Hot Temperature ; Humans ; Male ; Middle Aged ; Models, Biological ; Neurons, Afferent/*physiology ; Pain/*physiopathology ; Spinothalamic Tracts/*physiology
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  • 47
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    Specification of C/EBP function during Drosophila development by the bZIP basic region (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: The biologically relevant interactions of a transcription factor are those that are important for function in the organism. Here, a transgenic rescue assay was used to determine which molecular functions of Drosophila CCAAT/enhancer binding protein (C/EBP), a basic region-leucine zipper transcription factor, are required for it to fulfill its essential role during development. Chimeric proteins that contain the Drosophila C/EBP (DmC/EBP) basic region, a heterologous zipper, and a heterologous activation domain could functionally substitute for DmC/EBP. Mammalian C/EBPs were also functional in Drosophila. In contrast, 9 of 25 single amino acid substitutions in the basic region disrupted biological function. Thus, the conserved basic region specifies DmC/EBP activity in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rorth, P -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1878-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Embryology, Carnegie Institution of Washington, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997882" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Base Sequence ; Basic-Leucine Zipper Transcription Factors ; CCAAT-Enhancer-Binding Proteins ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/*physiology ; Drosophila/genetics/*growth & development ; Female ; G-Box Binding Factors ; *Leucine Zippers ; Male ; Molecular Sequence Data ; Nuclear Proteins/chemistry/genetics/*physiology ; Recombinant Fusion Proteins ; Transcription Factors/chemistry/genetics/*physiology ; Transcriptional Activation
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    Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: The 2;5 chromosomal translocation occurs in most anaplastic large-cell non-Hodgkin's lymphomas arising from activated T lymphocytes. This rearrangement was shown to fuse the NPM nucleolar phosphoprotein gene on chromosome 5q35 to a previously unidentified protein tyrosine kinase gene, ALK, on chromosome 2p23. In the predicted hybrid protein, the amino terminus of nucleophosmin (NPM) is linked to the catalytic domain of anaplastic lymphoma kinase (ALK). Expressed in the small intestine, testis, and brain but not in normal lymphoid cells, ALK shows greatest sequence similarity to the insulin receptor subfamily of kinases. Unscheduled expression of the truncated ALK may contribute to malignant transformation in these lymphomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, S W -- Kirstein, M N -- Valentine, M B -- Dittmer, K G -- Shapiro, D N -- Saltman, D L -- Look, A T -- CA 21765/CA/NCI NIH HHS/ -- KO8 CA 01702/CA/NCI NIH HHS/ -- P01 CA 20180/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122112" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain/enzymology ; Cell Transformation, Neoplastic ; Chromosome Walking ; Chromosomes, Human, Pair 2 ; Chromosomes, Human, Pair 5 ; Cloning, Molecular ; Gene Expression Regulation, Neoplastic ; Humans ; Intestine, Small/enzymology ; Lymphoma, Large-Cell, Anaplastic/chemistry/enzymology/*genetics ; Male ; Molecular Sequence Data ; Nuclear Proteins/chemistry/*genetics ; Phosphoproteins/chemistry/*genetics ; Promoter Regions, Genetic ; Protein-Tyrosine Kinases/chemistry/*genetics ; RNA, Messenger/genetics/metabolism ; Receptor Protein-Tyrosine Kinases ; Sequence Alignment ; Signal Transduction ; Testis/enzymology ; *Translocation, Genetic ; Tumor Cells, Cultured
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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    Implantation and the placenta: key pieces of the development puzzle (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: The mammalian embryo cannot develop without the placenta. Its specialized cells (trophoblast, endoderm, and extraembryonic mesoderm) form early in development. They attach the embryo to the uterus (implantation) and form vascular connections necessary for nutrient transport. In addition, the placenta redirects maternal endocrine, immune, and metabolic functions to the embryo's advantage. These complex activities are sensitive to disruption, as shown by the high incidence of early embryonic mortality and pregnancy diseases in humans, as well as the numerous peri-implantation lethal mutations in mice. Integration of molecular and developmental approaches has recently produced insights into the molecules that control these processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cross, J C -- Werb, Z -- Fisher, S J -- HD 22210/HD/NICHD NIH HHS/ -- HD 26732/HD/NICHD NIH HHS/ -- HD 30367/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1508-18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; Cell Differentiation ; Embryo Implantation/*physiology ; Embryonic and Fetal Development/genetics/*physiology ; Female ; Gene Expression Regulation, Developmental ; Hormones/physiology ; Humans ; Immune Tolerance ; Male ; Placenta/cytology/*physiology ; Trophoblasts/physiology ; Uterus/physiology
    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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    Birth control in Japan: realities and prognosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jitsukawa, M -- Djerassi, C -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1048-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Asia/Pacific Research Center, Stanford University, CA 94305-6055.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066442" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Legal ; Acquired Immunodeficiency Syndrome/transmission ; Condoms ; *Contraceptives, Oral/administration & dosage/adverse effects ; Drug Approval ; *Family Planning Services ; Female ; *Government Regulation ; Health Knowledge, Attitudes, Practice ; Humans ; Internationality ; Japan ; Legislation, Drug ; Male ; Mifepristone/administration & dosage ; Pregnancy ; Risk Assessment
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  • 52
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    Interaction of IL-2R beta and gamma c chains with Jak1 and Jak3: implications for XSCID and XCID (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: Interleukin-2 (IL-2) signaling requires the dimerization of the IL-2 receptor beta.(IL-2R beta) and common gamma (gamma c) chains. Mutations of gamma c can result in X-linked severe combined immunodeficiency (XSCID). IL-2, IL-4, IL-7 (whose receptors are known to contain gamma c), and IL-9 (whose receptor is shown here to contain gamma c) induced the tyrosine phosphorylation and activation of the Janus family tyrosine kinases Jak1 and Jak3. Jak1 and Jak3 associated with IL-2R beta and gamma c, respectively; IL-2 induced Jak3-IL-2R beta and increased Jak3-gamma c associations. Truncations of gamma c, and a gamma c, point mutation causing moderate X-linked combined immunodeficiency (XCID), decreased gamma c-Jak3 association. Thus, gamma c mutations in at least some XSCID and XCID patients prevent normal Jak3 activation, suggesting that mutations of Jak3 may result in an XSCID-like phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Johnston, J A -- Noguchi, M -- Kawamura, M -- Bacon, C M -- Friedmann, M -- Berg, M -- McVicar, D W -- Witthuhn, B A -- Silvennoinen, O -- P30 CA21765/CA/NCI NIH HHS/ -- R01 DK42932/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Enzyme Activation ; Humans ; Interleukin-2/pharmacology ; Janus Kinase 1 ; Janus Kinase 3 ; Mutation ; Phosphorylation ; Point Mutation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Interleukin-2/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/*immunology/metabolism ; Transfection ; Tyrosine/metabolism
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    A truncated erythropoietin receptor and cell death: a reanalysis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, Y -- Nakauchi, H -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):588-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8160019" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Base Sequence ; Cell Division ; Cell Line ; Erythropoietin/pharmacology ; Hematopoietic Stem Cells/cytology/*metabolism ; Humans ; Molecular Sequence Data ; Receptors, Erythropoietin/chemistry/genetics/*physiology ; Signal Transduction ; Transfection
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    Implications of FRA16A structure for the mechanism of chromosomal fragile site genesis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: Fragile sites are chemically induced nonstaining gaps in chromosomes. Different fragile sites vary in frequency in the population and in the chemistry of their induction. DNA sequences encompassing and including the rare, autosomal, folate-sensitive fragile site, FRA16A, were isolated by positional cloning. The molecular basis of FRA16A was found to be expansion of a normally polymorphic p(CCG)n repeat. This repeat was adjacent to a CpG island that was methylated in fragile site-expressing individuals. The FRA16A locus in individuals who do not express the fragile site is not a site of DNA methylation (imprinting), which suggests that the methylation associated with fragile sites may be a consequence and not a cause of their genesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nancarrow, J K -- Kremer, E -- Holman, K -- Eyre, H -- Doggett, N A -- Le Paslier, D -- Callen, D F -- Sutherland, G R -- Richards, R I -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1938-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cytogenetics and Molecular Genetics, Women's and Children's Hospital, North Adelaide, South Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009225" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Chromosome Fragile Sites ; *Chromosome Fragility ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human, Pair 16 ; Dinucleoside Phosphates/metabolism ; Female ; Fragile X Syndrome/genetics ; Humans ; Male ; Methylation ; Molecular Sequence Data ; Pedigree ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
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    Rates of mortality in populations of Caenorhabditis elegans (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtsinger, J W -- Fukui, H H -- Xiu, L -- Khazaeli, A -- Pletcher, S -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):826; author reply 828.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973640" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/physiology ; Drosophila/*physiology ; Female ; Male ; Mortality
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    Prophylactic vaccines, risk behavior change, and the probability of eradicating HIV in San Francisco (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: Theory is linked with data to assess the probability of eradicating human immunodeficiency virus (HIV) in San Francisco through the use of prophylactic vaccines. The necessary vaccine efficacy levels and population coverage levels for eradication are quantified. The likely impact of risk behavior changes on vaccination campaigns is assessed. The results show it is unlikely that vaccines will be able to eradicate HIV in San Francisco unless they are combined with considerable reductions in risk behaviors. Furthermore, if risk behavior increases as the result of a vaccination campaign, then vaccination could result in a perverse outcome by increasing the severity of the epidemic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blower, S M -- McLean, A R -- 1R29DA08153/DA/NIDA NIH HHS/ -- AI33831/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Epidemiology Department, School of Public Health, University of California at Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073289" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Adult ; Disease Outbreaks/prevention & control ; HIV Infections/epidemiology/*prevention & control ; *Homosexuality ; Humans ; Immunization Programs ; Male ; Probability ; *Risk-Taking ; San Francisco/epidemiology
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    Forward and reverse genetic approaches to behavior in the mouse (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: Modern molecular genetic and genomic approaches are revolutionizing the study of behavior in the mouse. "Reverse genetics" (from gene to phenotype) with targeted gene transfer provides a powerful tool to dissect behavior and has been used successfully to study the effects of null mutations in genes implicated in the regulation of long-term potentiation and spatial learning in mice. In addition, "forward genetics" (from phenotype to gene) with high-efficiency mutagenesis in the mouse can uncover unknown genes and has been used to isolate a behavioral mutant of the circadian system. With the recent availability of high-density genetic maps and physical mapping resources, positional cloning of virtually any mutation is now feasible in the mouse. Together, these approaches permit a molecular analysis of both known and previously unknown genes regulating behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830945/" 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/PMC3830945/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, J S -- Pinto, L H -- Vitaterna, M H -- EY08467/EY/NEI NIH HHS/ -- MH39592/MH/NIMH NIH HHS/ -- MH49241/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1724-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Circadian Rhythm/genetics ; Female ; *Genetic Techniques ; Genetics, Behavioral/*methods ; Learning ; Long-Term Potentiation ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mutagenesis
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    Requirement of a critical period of transcription for induction of a late phase of LTP (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: Repeated high-frequency trains of stimuli induce long-term potentiation (LTP) in the CA1 region that persists for up to 8 hours in hippocampal slices and for days in intact animals. This long time course has made LTP an attractive model for certain forms of long-term memory in the mammalian brain. A hallmark of long-term memory in the intact animal is a requirement for transcription, and thus whether the late phase of LTP (L-LTP) requires transcription was investigated here. With the use of different inhibitors, it was found in rat hippocampal slices that the induction of L-LTP [produced either by tetanic stimulation or by application of the cyclic adenosine monophosphate (cAMP) analog Sp-cAMPS (Sp-cyclic adenosine 3',5'-monophosphorothioate)] was selectively prevented when transcription was blocked immediately after tetanization or during application of cAMP. As with behavioral memory, this requirement for transcription had a critical time window. Thus, the late phase of LTP in the CA1 region requires transcription during a critical period, perhaps because cAMP-inducible genes must be expressed during this period.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nguyen, P V -- Abel, T -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066450" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/analogs & derivatives/metabolism/pharmacology ; Dactinomycin/pharmacology ; Dichlororibofuranosylbenzimidazole/pharmacology ; Electric Stimulation ; Evoked Potentials/drug effects ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Male ; Pyramidal Cells/metabolism ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; *Transcription, Genetic/drug effects
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    Enhanced aggressive behavior in mice lacking 5-HT1B receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: The neuromodulator serotonin (5-hydroxytryptamine, 5-HT) has been associated with mood disorders such as depression, anxiety, and impulsive violence. To define the contribution of 5-HT receptor subtypes to behavior, mutant mice lacking the 5-HT1B receptor were generated by homologous recombination. These mice did not exhibit any obvious developmental or behavioral defects. However, the hyperlocomotor effect of the 5-HT1A/1B agonist RU24969 was absent in mutant mice, indicating that this effect is mediated by 5-HT1B receptors. Moreover, when confronted with an intruder, mutant mice attacked the intruder faster and more intensely than did wild-type mice, suggesting the participation of 5-HT1B receptors in aggressive behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saudou, F -- Amara, D A -- Dierich, A -- LeMeur, M -- Ramboz, S -- Segu, L -- Buhot, M C -- Hen, R -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1875-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, U184 de l'INSERM, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091214" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; Brain Chemistry ; Chimera ; Female ; Indoles/pharmacology ; Male ; Mice ; Motor Activity/drug effects ; Mutation ; Pindolol/analogs & derivatives/metabolism ; Receptor, Serotonin, 5-HT1B ; Receptors, Serotonin/analysis/genetics/*physiology ; Recombination, Genetic ; Serotonin Receptor Agonists/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Adequate supplies of fruits and vegetables (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1303.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973710" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Diet ; Female ; *Fruit ; *Fungicides, Industrial/toxicity ; Humans ; Male ; Mice ; United States ; United States Environmental Protection Agency ; *Vegetables
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    Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darnell, J E Jr -- Kerr, I M -- Stark, G R -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1415-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197455" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/*metabolism ; Genes ; Genetic Complementation Test ; Humans ; Interferon-Stimulated Gene Factor 3 ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Mutation ; Protein-Tyrosine Kinases/metabolism ; Regulatory Sequences, Nucleic Acid ; *Signal Transduction ; Transcription Factors/*metabolism ; *Transcriptional Activation
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    Modulation of epithelial cell growth by intraepithelial gamma delta T cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: The role played in immune surveillance by gamma delta T cells residing in various epithelia has not been clear. It is shown here that activated gamma delta T cells obtained from skin and intestine express the epithelial cell mitogen keratinocyte growth factor (KGF). In contrast, intraepithelial alpha beta T cells, as well as all lymphoid alpha beta and gamma delta T cell populations tested, did not produce KGF or promote the growth of cultured epithelial cells. These results suggest that intraepithelial gamma delta T cells function in surveillance and in repair of damaged epithelial tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Dendritic Cells/*physiology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*biosynthesis/genetics ; Keratinocytes/*cytology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; *Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocyte Subsets/immunology/metabolism/*physiology
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    Population policy options in the developing world (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: The population of the developing world is currently expanding at the unprecedented rate of more than 800 million per decade, and despite anticipated reductions in growth during the 21st century, its size is expected to increase from 4.3 billion today to 10.2 billion in 2100. Past efforts to curb this growth have almost exclusively focused on the implementation of family planning programs to provide contraceptive information, services, and supplies. These programs have been partially successful in reducing birth rates. Further investments in them will have an additional but limited impact on population growth; therefore, other policy options, in particular measures to reduce high demand for births and limit population momentum, are needed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bongaarts, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):771-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Division, Population Council, New York, NY 10017.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303293" target="_blank"〉PubMed〈/a〉
    Keywords: Contraception ; *Developing Countries ; Family Characteristics ; *Family Planning Policy ; Female ; Humans ; Male ; *Population Control ; *Population Growth
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    Reversion of the mouse pink-eyed unstable mutation induced by low doses of x-rays (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Deletions and other genome rearrangements can be caused by radiation and are associated with carcinogenesis and inheritable diseases. The pink-eyed unstable (p(un)) mutation in the mouse is caused by a gene duplication and reverts to wild type by deletion of one copy. Reversion events in the mouse embryo were detected as black spots on the fur of the animals or microscopically as partially black hair in a background of colorless hair. The frequency of partially black hair was increased by x-rays at very low doses. A linear dose-response relation was found between 1 and 100 centigray.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schiestl, R H -- Khogali, F -- Carls, N -- ES06593/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1573-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Toxicology, Harvard School of Public Health, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Radiation ; Embryo, Mammalian/radiation effects ; Female ; *Gene Deletion ; Hair Color/genetics/radiation effects ; Male ; Maternal Exposure ; Melanocytes/radiation effects ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Multigene Family ; Mutagenicity Tests ; Mutation/*radiation effects
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    Digenic retinitis pigmentosa due to mutations at the unlinked peripherin/RDS and ROM1 loci (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: In spite of recent advances in identifying genes causing monogenic human disease, very little is known about the genes involved in polygenic disease. Three families were identified with mutations in the unlinked photoreceptor-specific genes ROM1 and peripherin/RDS, in which only double heterozygotes develop retinitis pigmentosa (RP). These findings indicate that the allelic and nonallelic heterogeneity known to be a feature of monogenic RP is complicated further by interactions between unlinked mutations causing digenic RP. Recognition of the inheritance pattern exemplified by these three families might facilitate the identification of other examples of digenic inheritance in human disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kajiwara, K -- Berson, E L -- Dryja, T P -- EY00169/EY/NEI NIH HHS/ -- EY08683/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1604-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berman-Gund Laboratory for the Study of Retinal Degenerations, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202715" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Electroretinography ; Eye Proteins/chemistry/*genetics ; Female ; Genes, Dominant ; Genes, Recessive ; Genetic Linkage ; Heterozygote ; Humans ; Intermediate Filament Proteins/chemistry/*genetics ; Male ; *Membrane Glycoproteins ; Membrane Proteins/chemistry/*genetics ; Molecular Sequence Data ; Mutation ; *Nerve Tissue Proteins ; Pedigree ; Peripherins ; Retinitis Pigmentosa/*genetics ; Rod Cell Outer Segment/chemistry ; Tetraspanins
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    Prevention of T cell anergy by signaling through the gamma c chain of the IL-2 receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: When stimulated through their antigen receptor without requisite costimulation, T cells enter a state of antigen-specific unresponsiveness termed anergy. In this study, signaling through the common gamma chain of the interleukin-2 (IL-2), IL-4, and IL-7 receptors in the presence of antigen was found to be sufficient to prevent the induction of anergy. After culture with IL-2, IL-4, or IL-7, Jak3 kinase was tyrosine-phosphorylated, which correlated with the prevention of anergy. Therefore, a signal through the common gamma chain may regulate the decision of T cells to either clonally expand or enter a state of anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boussiotis, V A -- Barber, D L -- Nakarai, T -- Freeman, G J -- Gribben, J G -- Bernstein, G M -- D'Andrea, A D -- Ritz, J -- Nadler, L M -- AI 35225/AI/NIAID NIH HHS/ -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1039-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973657" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Clonal Anergy/*immunology ; Clone Cells ; HLA-DR7 Antigen/immunology ; Humans ; Interleukins/immunology ; Janus Kinase 3 ; Lymphocyte Activation ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Interleukin-2/immunology/*metabolism ; *Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Necrosis Factor-alpha/immunology
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    Gem: an induced, immediate early protein belonging to the Ras family (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: A gene encoding a 35-kilodalton guanosine triphosphate (GTP)-binding protein, Gem, was cloned from mitogen-induced human peripheral blood T cells. Gem and Rad, the product of a gene overexpressed in skeletal muscle in individuals with Type II diabetes, constitute a new family of Ras-related GTP-binding proteins. The distinct structural features of this family include the G3 GTP-binding motif, extensive amino- and carboxyl-terminal extensions beyond the Ras-related domain, and a motif that determines membrane association. Gem was transiently expressed in human peripheral blood T cells in response to mitogenic stimulation; the protein was phosphorylated on tyrosine residues and localized to the cytosolic face of the plasma membrane. Deregulated Gem expression prevented proliferation of normal and transformed 3T3 cells. These results suggest that Gem is a regulatory protein, possibly participating in receptor-mediated signal transduction at the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maguire, J -- Santoro, T -- Jensen, P -- Siebenlist, U -- Yewdell, J -- Kelly, K -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):241-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7912851" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CD4-Positive T-Lymphocytes/metabolism ; Cell Death ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Genes, ras ; Guanosine Triphosphate/metabolism ; Humans ; Immediate-Early Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; *Monomeric GTP-Binding Proteins ; Mutation ; RNA, Messenger/genetics/metabolism ; Transfection ; *ras Proteins
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    Requirement of human renal water channel aquaporin-2 for vasopressin-dependent concentration of urine (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: Concentration of urine in mammals is regulated by the antidiuretic hormone vasopressin. Binding of vasopressin to its V2 receptor leads to the insertion of water channels in apical membranes of principal cells in collecting ducts. In nephrogenic diabetes insipidus (NDI), the kidney fails to concentrate urine in response to vasopressin. A male patient with an autosomal recessive form of NDI was found to be a compound heterozygote for two mutations in the gene encoding aquaporin-2, a water channel. Functional expression studies in Xenopus oocytes revealed that each mutation resulted in nonfunctional water channel proteins. Thus, aquaporin-2 is essential for vasopressin-dependent concentration of urine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deen, P M -- Verdijk, M A -- Knoers, N V -- Wieringa, B -- Monnens, L A -- van Os, C H -- van Oost, B A -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):92-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology, University of Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140421" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aquaporin 2 ; Aquaporin 6 ; *Aquaporins ; Base Sequence ; Cloning, Molecular ; Deamino Arginine Vasopressin/*pharmacology ; Diabetes Insipidus/*genetics/physiopathology ; Female ; Genes, Recessive ; Heterozygote ; Humans ; Kidney/metabolism/*physiology ; *Kidney Concentrating Ability ; Male ; Membrane Proteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; Oocytes ; Pedigree ; Point Mutation ; Protein Structure, Secondary ; RNA, Complementary/genetics ; Water/metabolism ; Xenopus laevis
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    Electromagnetic fields. Breast cancer link claimed, criticized (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, G -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1658.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209240" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*etiology ; Electromagnetic Fields/*adverse effects ; Female ; Humans ; Male ; Melatonin/biosynthesis ; *Neoplasms, Radiation-Induced ; *Occupational Exposure ; Pineal Gland/metabolism/radiation effects
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    Reconstitution of an operational MHC class II compartment in nonantigen-presenting cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Professional antigen-presenting cells (APCs) have a distinct compartment in which class II molecules are proposed to acquire antigenic peptides. Genetic evidence suggests that human leukocyte antigen (HLA)-DM, an unusual class II molecule, participates in this process. Peptide acquisition was reconstituted in nonprofessional APCs by transfection of class II, invariant chain (li), and H-2M, the murine equivalent of DM. The H-2M heterodimer appeared in an endosomal compartment, not at the cell surface, and the localization was independent of li. The data presented show that H-2M, class II, and li are the minimally required components for efficient formation of stable class II-peptide complexes, and thus for a functional class II compartment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlsson, L -- Peleraux, A -- Lindstedt, R -- Liljedahl, M -- Peterson, P A -- AI-26610/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1569-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985028" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antigen Presentation ; Antigen-Presenting Cells/immunology ; *Antigens, Differentiation, B-Lymphocyte ; B-Lymphocytes/immunology ; Cell Line ; Cell Membrane/immunology ; Endosomes/*immunology ; Fluorescent Antibody Technique ; H-2 Antigens/analysis/genetics/*metabolism ; HLA-DR3 Antigen/*metabolism ; HeLa Cells ; Histocompatibility Antigens Class II/*metabolism ; Humans ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prevention of lipopolysaccharide-induced lethal toxicity by tyrosine kinase inhibitors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-27
    Description: Septic shock results from excessive stimulation of the host immune system, especially macrophages, by lipopolysaccharide (LPS), or endotoxin, which resides on the outer membrane of bacteria. Protein tyrosine kinase inhibitors of the tyrphostin AG 126 family protect mice against LPS-induced lethal toxicity. The protection correlates with the ability of these agents to block LPS-induced production of tumor necrosis factor alpha (TNF-alpha) and nitric oxide in macrophages as well as LPS-induced production of TNF-alpha in vivo. Furthermore, this inhibitory effect correlated with the potency of AG 126 to block LPS-induced tyrosine phosphorylation of a p42MAPK protein substrate in the murine macrophage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novogrodsky, A -- Vanichkin, A -- Patya, M -- Gazit, A -- Osherov, N -- Levitzki, A -- New York, N.Y. -- Science. 1994 May 27;264(5163):1319-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Felsenstein Medical Research Center, Petach Tikva, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzylidene Compounds/*pharmacology ; Biological Assay ; Cell Line ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Enzyme-Linked Immunosorbent Assay ; Female ; Lipopolysaccharides/*toxicity ; Macrophage Activation ; Macrophages, Peritoneal/*drug effects/metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 1 ; Nitric Oxide/*biosynthesis ; Nitriles/*pharmacology ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/analysis/*biosynthesis/toxicity ; *Tyrphostins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Risking everything? Risk behavior, behavior change, and AIDS (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: Inquiry into the determinants of risk-related sexual behavior is important for the development of interventions to reduce the incidence of new cases of human immunodeficiency virus infection. Recent social and behavioral research has revealed much about the individual and social factors influencing risk-taking. Findings from these studies have been important in the development of new educational and community-based interventions for communities at risk in the developed and developing worlds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aggleton, P -- O'Reilly, K -- Slutkin, G -- Davies, P -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):341-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Global Programme on AIDS, World Health Organization, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023156" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/epidemiology/prevention & ; control/*transmission ; Cultural Characteristics ; Developing Countries ; Disease Outbreaks ; Female ; Global Health ; Humans ; Male ; *Risk-Taking ; *Sexual Behavior ; Socioeconomic Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Activation of the myogenic lineage by MEF2A, a factor that induces and cooperates with MyoD (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: Muscle enhancer factor-2A (MEF2A), a member of the MADS family, induced myogenic development when ectopically expressed in clones of nonmuscle cells of human clones, a function previously limited to the muscle basic helix-loop-helix (bHLH) proteins. During myogenesis, MEF2A and bHLH proteins cooperatively activate skeletal muscle genes and physically interact through the MADS domain of MEF2A and the three myogenic amino acids of the muscle bHLH proteins. Thus, skeletal myogenesis is mediated by two distinct families of mutually inducible and interactive muscle transcription factors, either of which can initiate the developmental cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaushal, S -- Schneider, J W -- Nadal-Ginard, B -- Mahdavi, V -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1236-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973707" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Differentiation ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; *Gene Expression Regulation ; Genes, Reporter ; Haplorhini ; Helix-Loop-Helix Motifs ; Humans ; MADS Domain Proteins ; MEF2 Transcription Factors ; Mice ; Molecular Sequence Data ; Muscle, Skeletal/*cytology/metabolism ; MyoD Protein/biosynthesis/*metabolism ; Myogenic Regulatory Factors ; Myogenin/biosynthesis/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    CD26 antigen and HIV fusion? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Broder, C C -- Nussbaum, O -- Gutheil, W G -- Bachovchin, W W -- Berger, E A -- New York, N.Y. -- Science. 1994 May 20;264(5162):1156-9; author reply 1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909959" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*physiology ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Base Sequence ; *Cell Fusion ; Cell Line ; Dipeptidyl Peptidase 4 ; Gene Products, env/*physiology ; Giant Cells/physiology ; HIV-1/*physiology ; Humans ; Hybrid Cells ; Molecular Sequence Data
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 75
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    Characterization of type I receptors for transforming growth factor-beta and activin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: Transforming growth factor-beta (TGF-beta) and activin exert their effects by binding to heteromeric complexes of type I and type II receptors. The type II receptors for TGF-beta and activin are transmembrane serine-threonine kinases; a series of related receptors, denoted activin receptor-like kinase (ALK) 1 to 5, have recently been identified, and ALK-6 is described here. ALK-5 has been shown to be a functional TGF-beta type I receptor. A systematic analysis revealed that most ALKs formed heteromeric complexes with the type II receptors for TGF-beta and activin after overexpression in COS cells; however, among the six ALKs, only ALK-5 was a functional TGF-beta type I receptor for activation of plasminogen activator inhibitor-1, and only ALK-2 and ALK-4 bound activin with high affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉ten Dijke, P -- Yamashita, H -- Ichijo, H -- Franzen, P -- Laiho, M -- Miyazono, K -- Heldin, C H -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140412" target="_blank"〉PubMed〈/a〉
    Keywords: Activin Receptors ; Activins ; Amino Acid Sequence ; Animals ; Bone Morphogenetic Protein Receptors, Type I ; Cell Line ; Inhibins/*metabolism ; Ligands ; Mice ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Receptors, Growth Factor/chemistry/*metabolism ; Receptors, Transforming Growth Factor beta/chemistry/*metabolism ; Transforming Growth Factor beta/*metabolism
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    Linkage analysis of IL4 and other chromosome 5q31.1 markers and total serum immunoglobulin E concentrations (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: Sib-pair analysis of 170 individuals from 11 Amish families revealed evidence for linkage of five markers in chromosome 5q31.1 with a gene controlling total serum immunoglobulin E (IgE) concentration. No linkage was found between these markers and specific IgE antibody concentrations. Analysis of total IgE within a subset of 128 IgE antibody-negative sib pairs confirmed evidence for linkage to 5q31.1, especially to the interleukin-4 gene (IL4). A combination of segregation and maximum likelihood analyses provided further evidence for this linkage. These analyses suggest that IL4 or a nearby gene in 5q31.1 regulates IgE production in a nonantigen-specific (noncognate) fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsh, D G -- Neely, J D -- Breazeale, D R -- Ghosh, B -- Freidhoff, L R -- Ehrlich-Kautzky, E -- Schou, C -- Krishnaswamy, G -- Beaty, T H -- 1 P41 RR03655/RR/NCRR NIH HHS/ -- AI20059/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1152-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Asthma and Allergy Center, School of Medicine, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178175" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Allergens/immunology ; Base Sequence ; Child ; Child, Preschool ; *Chromosomes, Human, Pair 5 ; Female ; Genes, MHC Class II ; *Genetic Linkage ; Genetic Markers ; Humans ; Hypersensitivity, Immediate/genetics ; Immunoglobulin E/*blood ; Interleukin-4/*genetics ; Likelihood Functions ; Lod Score ; Male ; Middle Aged ; Molecular Sequence Data
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-01
    Description: Deletion of the promoter and the first exon of the DNA polymerase beta gene (pol beta) in the mouse germ line results in a lethal phenotype. With the use of the bacteriophage-derived, site-specific recombinase Cre in a transgenic approach, the same mutation can be selectively introduced into a particular cellular compartment-in this case, T cells. The impact of the mutation on those cells can then be analyzed because the mutant animals are viable.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, H -- Marth, J D -- Orban, P C -- Mossmann, H -- Rajewsky, K -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Nucleotidyltransferases/genetics/metabolism ; DNA Polymerase I/*genetics/metabolism ; Female ; *Gene Deletion ; Genetic Engineering/*methods ; Homozygote ; *Integrases ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Recombination, Genetic ; Stem Cells/enzymology ; T-Lymphocytes/*enzymology ; Transfection ; *Viral Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: A gene involved in psoriasis susceptibility was localized to the distal region of human chromosome 17q as a result of a genome-wide linkage analysis with polymorphic microsatellites and eight multiply affected psoriasis kindreds. In the family which showed the strongest evidence for linkage, the recombination fraction between a psoriasis susceptibility locus and D17S784 was 0.04 with a maximum two-point lod score of 5.33. There was also evidence for genetic heterogeneity and although none of the linked families showed any association with HLA-Cw6, two unlinked families showed weak levels of association. This study demonstrates that in some families, psoriasis susceptibility is due to variation at a single major genetic locus other than the human lymphocyte antigen locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomfohrde, J -- Silverman, A -- Barnes, R -- Fernandez-Vina, M A -- Young, M -- Lory, D -- Morris, L -- Wuepper, K D -- Stastny, P -- Menter, A -- P01-AI2327/AI/NIAID NIH HHS/ -- R01 HL47145/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1141-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235-8591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178173" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; DNA Primers ; DNA, Satellite/genetics ; Disease Susceptibility ; Female ; Genetic Linkage ; Genetic Markers ; HLA-C Antigens/genetics ; Haplotypes ; Humans ; Lod Score ; Male ; Molecular Sequence Data ; Pedigree ; Polymorphism, Genetic ; Psoriasis/*genetics ; Software
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    Fertilization and ion channels (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nuccitelli, R -- Ferguson, J E -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):988.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8310299" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Female ; *Fertilization ; Male ; Oocytes/*physiology ; Sodium Channels/*physiology ; Spermatozoa/metabolism ; Xenopus laevis
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    Long-term behavioral recovery in parkinsonian rats by an HSV vector expressing tyrosine hydroxylase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: One therapeutic approach to treating Parkinson's disease is to convert endogenous striatal cells into levo-3,4-dihydroxyphenylalanine (L-dopa)-producing cells. A defective herpes simplex virus type 1 vector expressing human tyrosine hydroxylase was delivered into the partially denervated striatum of 6-hydroxydopamine-lesioned rats, used as a model of Parkinson's disease. Efficient behavioral and biochemical recovery was maintained for 1 year after gene transfer. Biochemical recovery included increases in both striatal tyrosine hydroxylase enzyme activity and in extracellular dopamine concentrations. Persistence of human tyrosine hydroxylase was revealed by expression of RNA and immunoreactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" 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/PMC2638002/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉During, M J -- Naegele, J R -- O'Malley, K L -- Geller, A I -- EY09749/EY/NEI NIH HHS/ -- NS06208/NS/NINDS NIH HHS/ -- NS28227/NS/NINDS NIH HHS/ -- R01 NS034025/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1399-403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7669103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Corpus Striatum/*enzymology/metabolism ; Denervation ; Disease Models, Animal ; Dopamine/metabolism ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Humans ; Levodopa/metabolism ; Male ; Molecular Sequence Data ; *Motor Activity ; Neurons/enzymology ; Parkinson Disease/metabolism/*therapy ; Rats ; Rats, Sprague-Dawley ; Simplexvirus/*genetics ; Tyrosine 3-Monooxygenase/*genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Efficient neutralization of primary isolates of HIV-1 by a recombinant human monoclonal antibody (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The ability of antibodies to neutralize diverse primary isolates of human immunodeficiency virus-type 1 in vitro has been questioned, with implications for the likely efficacy of vaccines. A recombinant human antibody to envelope glycoprotein gp120 was generated and used to show that primary isolates are not refractory to antibody neutralization. The recombinant antibody neutralized more than 75 percent of the primary isolates tested at concentrations that could be achieved by passive immunization, for example, to interrupt maternal-fetal transmission of virus. The broad specificity and efficacy of the antibody implies the conservation of a structural feature on gp120, which could be important in vaccine design.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burton, D R -- Pyati, J -- Koduri, R -- Sharp, S J -- Thornton, G B -- Parren, P W -- Sawyer, L S -- Hendry, R M -- Dunlop, N -- Nara, P L -- AI27742/AI/NIAID NIH HHS/ -- AI33292/AI/NIAID NIH HHS/ -- AI35168/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1024-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973652" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Acquired Immunodeficiency Syndrome/virology ; Amino Acid Sequence ; Antibodies, Monoclonal/*immunology ; Antibody Specificity ; HIV Antibodies/*immunology ; HIV Core Protein p24/analysis ; HIV Envelope Protein gp120/*immunology ; HIV-1/*immunology/isolation & purification ; Humans ; Immunization, Passive ; Immunoglobulin Fab Fragments/immunology ; Immunoglobulin G/immunology ; Infant ; Infant, Newborn ; Male ; Molecular Sequence Data ; Neutralization Tests ; Recombinant Proteins/immunology
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    Manic depression. Highs and lows on the research roller coaster (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1693-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209248" target="_blank"〉PubMed〈/a〉
    Keywords: Bipolar Disorder/*genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Chromosomes, Human, Pair 18 ; Female ; Genetic Markers ; *Genetic Techniques ; *Genome, Human ; Humans ; Lod Score ; Male
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  • 83
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    On the trail of a second susceptibility gene (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, C -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1798.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091206" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Female ; Genes, Tumor Suppressor ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Male ; Mutation
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    A hearty endorsement for aspirin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aldhous, P -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):24.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272863" target="_blank"〉PubMed〈/a〉
    Keywords: Aspirin/*therapeutic use ; Cardiovascular Diseases/*prevention & control ; Female ; Humans ; Male ; Meta-Analysis as Topic ; Risk Factors ; Thrombosis/*prevention & control ; United States ; United States Food and Drug Administration
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    The mating of a fly (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: Courtship in Drosophila is influenced by a wide variety of genes, in that many different kinds of pleiotropic mutations lead to defective courtship. This may seem to be a truism, but the broad temporal and spatial expression of most of the fly's "neuro genes" makes it difficult to exclude elements of such genes' actions as materially underlying reproductive behavior. "Courtship genes" that seem to play more particular roles were originally identified as sensory, learning, or rhythm mutations; their reproductive abnormalities have been especially informative for revealing components of male or female actions that might otherwise have gone unnoticed. Further behavioral mutations seemed originally to be courtship-specific, turned out not to have that property, and have led to a broadened perspective on the nature and action of Drosophila's sex-determination genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, J C -- GM-21473/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1702-14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254-9110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/anatomy & histology/*genetics/physiology ; Female ; *Genes, Insect ; Male ; Mutation ; Nervous System Physiological Phenomena ; Phenotype ; Sex Characteristics ; Sex Determination Analysis ; *Sexual Behavior, Animal
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  • 86
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    Human severe combined immunodeficiency due to a defect in ZAP-70, a T cell tyrosine kinase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: A homozygous mutation in the kinase domain of ZAP-70, a T cell receptor-associated protein tyrosine kinase, produced a distinctive form of human severe combined immunodeficiency. Manifestations of this disorder included profound immunodeficiency, absence of peripheral CD8+ T cells, and abundant peripheral CD4+ T cells that were refractory to T cell receptor-mediated activation. These findings demonstrate that ZAP-70 is essential for human T cell function and suggest that CD4+ and CD8+ T cells depend on different intracellular signaling pathways to support their development or survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elder, M E -- Lin, D -- Clever, J -- Chan, A C -- Hope, T J -- Weiss, A -- Parslow, T G -- AI29313/AI/NIAID NIH HHS/ -- GM43574/GM/NIGMS NIH HHS/ -- RR01271/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California, San Francisco 94143-0110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202712" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cloning, Molecular ; Female ; Frameshift Mutation ; Gene Deletion ; Homozygote ; Humans ; Infant ; Male ; Molecular Sequence Data ; Polymerase Chain Reaction ; Protein-Tyrosine Kinases/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Transfection ; Tumor Cells, Cultured ; ZAP-70 Protein-Tyrosine Kinase
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  • 87
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    The paradox of critical mass for women in science (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etzkowitz, H -- Kemelgor, C -- Neuschatz, M -- Uzzi, B -- Alonzo, J -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):51-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sociology Board, State University of New York at Purchase 10577.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939644" target="_blank"〉PubMed〈/a〉
    Keywords: *Education, Graduate ; *Faculty ; Female ; Humans ; Male ; *Science ; Universities ; *Women ; Women, Working
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    National Institutes of Health. New law brings affirmative action to clinical research (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):602.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303263" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials, Phase III as Topic/*legislation & jurisprudence/methods ; Female ; Humans ; Male ; *Minority Groups ; *National Institutes of Health (U.S.) ; United States ; *Women's Health
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-05
    Description: Mammalian cells respond to endotoxic lipopolysaccharide (LPS) by activation of protein kinase cascades that lead to new gene expression. A protein kinase, p38, that was tyrosine phosphorylated in response to LPS, was cloned. The p38 enzyme and the product of the Saccharomyces cerevisiae HOG1 gene, which are both members of the mitogen-activated protein (MAP) kinase family, have sequences at and adjacent to critical phosphorylation sites that distinguish these proteins from most other MAP kinase family members. Both HOG1 and p38 are tyrosine phosphorylated after extracellular changes in osmolarity. These findings link a signaling pathway in mammalian cells with a pathway in yeast that is responsive to physiological stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, J -- Lee, J D -- Bibbs, L -- Ulevitch, R J -- AI15136/AI/NIAID NIH HHS/ -- GM28485/GM/NIGMS NIH HHS/ -- GM37696/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):808-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7914033" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*chemistry/genetics ; Cell Line ; Endotoxins/*pharmacology ; Genetic Complementation Test ; Lipopolysaccharides/pharmacology ; Macrophages, Peritoneal/enzymology ; Mice ; Mice, Inbred C3H ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Osmotic Pressure ; Paclitaxel/pharmacology ; Saccharomyces cerevisiae/genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Amino Acid ; Water-Electrolyte Balance/*physiology ; p38 Mitogen-Activated Protein Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    MHC class I expression in mice lacking the proteasome subunit LMP-7 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-26
    Description: Proteasomes degrade endogenous proteins. Two subunits, LMP-2 and LMP-7, are encoded in a region of the major histocompatibility complex (MHC) that is critical for class I-restricted antigen presentation. Mice with a targeted deletion of the gene encoding LMP-7 have reduced levels of MHC class I cell-surface expression and present the endogenous antigen HY inefficiently; addition of peptides to splenocytes deficient in LMP-7 restores wild-type class I expression levels. This demonstrates the involvement of LMP-7 in the MHC class I presentation pathway and suggests that LMP-7 functions as an integral part of the peptide supply machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fehling, H J -- Swat, W -- Laplace, C -- Kuhn, R -- Rajewsky, K -- Muller, U -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1234-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066463" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Base Sequence ; Carrier Proteins/genetics ; *Cysteine Endopeptidases ; Female ; Gene Deletion ; H-2 Antigens/*biosynthesis/immunology ; H-Y Antigen/immunology ; Lymphocytes/immunology ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Multienzyme Complexes ; Proteasome Endopeptidase Complex ; Proteins/genetics/*physiology
    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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  • 91
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    Molecular basis of mammalian sexual determination: activation of Mullerian inhibiting substance gene expression by SRY (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: The pathway of male sexual development in mammals is initiated by SRY, a gene on the short arm of the Y chromosome. Its expression in the differentiating gonadal ridge directs testicular morphogenesis, characterized by elaboration of Mullerian inhibiting substance (MIS) and testosterone. SRY and MIS each belong to conserved gene families that function in the control of growth and differentiation. Structural and biochemical studies of the DNA binding domain of SRY (the HMG box) revealed a protein-DNA interaction consisting of partial side chain intercalation into a widened minor groove. Functional studies of SRY in a cell line from embryonic gonadal ridge demonstrated activation of a gene-regulatory pathway leading to expression of MIS. SRY molecules containing mutations associated with human sex reversal have altered structural interactions with DNA and failed to induce transcription of MIS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haqq, C M -- King, C Y -- Ukiyama, E -- Falsafi, S -- Haqq, T N -- Donahoe, P K -- Weiss, M A -- GM51558/GM/NIGMS NIH HHS/ -- HD30812/HD/NICHD NIH HHS/ -- P30HD28138/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1494-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pediatric Surgical Research Laboratory, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985018" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Mullerian Hormone ; Base Sequence ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Female ; *Gene Expression Regulation, Developmental ; Genitalia, Male/*embryology ; *Glycoproteins ; Growth Inhibitors/biosynthesis/*genetics ; Humans ; Male ; Models, Biological ; Models, Molecular ; Molecular Sequence Data ; Mullerian Ducts ; *Nuclear Proteins ; Sex Differentiation/*genetics ; Sex-Determining Region Y Protein ; Testicular Hormones/biosynthesis/*genetics ; Transcription Factors/chemistry/*genetics/metabolism
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  • 92
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    Association of polyomavirus middle tumor antigen with 14-3-3 proteins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-22
    Description: To carry out its transformation function, the middle tumor antigen (MT) of murine polyomavirus associates with a number of cellular proteins involved in regulation of cell proliferation, including pp60c-Src, phosphatidylinositol 3-kinase, protein phosphatase 2A, Src homologous and collagen protein and growth factor receptor-binding protein 2. Here, two additional MT-associated proteins were identified as members of the 14-3-3 family of proteins. Yeast homologs of 14-3-3 proteins have recently been shown to play a role in the timing of mitosis. Thus, regulation of 14-3-3 protein function by MT may contribute to the development of neoplasia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pallas, D C -- Fu, H -- Haehnel, L C -- Weller, W -- Collier, R J -- Roberts, T M -- CA30002/CA/NCI NIH HHS/ -- CA45285/CA/NCI NIH HHS/ -- CA50661/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036498" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; 3T3 Cells ; Adenosine Diphosphate Ribose/metabolism ; Amino Acid Sequence ; Animals ; Antigens, Polyomavirus Transforming/immunology/*metabolism ; *Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Humans ; Immune Sera ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/isolation & purification/*metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Precipitin Tests ; *Tyrosine 3-Monooxygenase
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  • 93
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    Mutation of a mutL homolog in hereditary colon cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: Some cases of hereditary nonpolyposis colorectal cancer (HNPCC) are due to alterations in a mutS-related mismatch repair gene. A search of a large database of expressed sequence tags derived from random complementary DNA clones revealed three additional human mismatch repair genes, all related to the bacterial mutL gene. One of these genes (hMLH1) resides on chromosome 3p21, within 1 centimorgan of markers previously linked to cancer susceptibility in HNPCC kindreds. Mutations of hMLH1 that would disrupt the gene product were identified in such kindreds, demonstrating that this gene is responsible for the disease. These results suggest that defects in any of several mismatch repair genes can cause HNPCC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papadopoulos, N -- Nicolaides, N C -- Wei, Y F -- Ruben, S M -- Carter, K C -- Rosen, C A -- Haseltine, W A -- Fleischmann, R D -- Fraser, C M -- Adams, M D -- CA35494/CA/NCI NIH HHS/ -- CA47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1625-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128251" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; *Adenosine Triphosphatases ; Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics ; Base Sequence ; Carrier Proteins ; Chromosome Mapping ; *Chromosomes, Human, Pair 3 ; Codon ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; *DNA Repair ; *DNA-Binding Proteins ; *Escherichia coli Proteins ; Female ; Frameshift Mutation ; *Genes ; Genetic Markers ; Humans ; Male ; Molecular Sequence Data ; MutS Homolog 2 Protein ; Mutation ; Neoplasm Proteins/chemistry/*genetics ; Nuclear Proteins ; Open Reading Frames ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/genetics ; Sequence Deletion ; Tumor Cells, Cultured
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  • 94
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    Population policy options (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-06
    Description: In the review by Kristie Macrakis of Beyond the Wall: Memoirs of an East and West German Spy by Werner Stiller, with Jefferson Adams (editor and translator) [Brassey's (US), McLean, VA, 1992; Maxwell Macmillan, London, UK, 1992] (17 Dec., p. 1908), it is stated that physicist Rolf Dobbertin, who denies any spying, was "sent to Paris in 1956 to study at the expense of the Stasi," was "sentenced to 12 years in prison," and "sat in a French jail for five years before he was released in 1991." Legal documents show that Dobbertin, who was arrested in January 1979 for acts of "communication with agents of a foreign power, dealings that could be harmful [intelligence de nature a nuire] to the military or diplomatic situation of France or to its essential economic interest," was jailed until May 1983. He was subsequently tried in 1990 and sentenced to 12 years in prison, but was acquitted of the above charge by a special Assize Court in a second trial in November 1991. According to Dobbertin, he studied continuously at the University of Rostock from 1952 until 1958, and then taught at the University of Berlin for one year before beginning his work in 1959 at the Centre Nationale de la Recherche Scientifigue in France, where he continues to be employed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Treisman, M -- New York, N.Y. -- Science. 1994 May 6;264(5160):760.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171327" target="_blank"〉PubMed〈/a〉
    Keywords: *Developing Countries ; *Family Characteristics ; Female ; Humans ; Male ; *Population Control ; *Social Security
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  • 95
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    ZAP-70 deficiency in an autosomal recessive form of severe combined immunodeficiency (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: Protein tyrosine kinases (PTKs) play an integral role in T cell activation and differentiation. Defects in the Src-family PTKs in mice and in T cell lines have resulted in variable defects in thymic development and in T cell antigen receptor (TCR) signal transduction. Here, three siblings are described with an autosomal recessive form of severe combined immunodeficiency disease (SCID) in which ZAP-70, a non-Src PTK, is absent as a result of mutations in the ZAP-70 gene. This absence is associated with defects in TCR signal transduction, suggesting an important functional role for ZAP-70.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, A C -- Kadlecek, T A -- Elder, M E -- Filipovich, A H -- Kuo, W L -- Iwashima, M -- Parslow, T G -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1599-601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202713" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Cell Line ; Child ; Female ; Gene Deletion ; *Genes, Recessive ; Humans ; Lymphocyte Activation ; Male ; Molecular Sequence Data ; Mutation ; Point Mutation ; Protein-Tyrosine Kinases/deficiency/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; ZAP-70 Protein-Tyrosine Kinase
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  • 96
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    Restoration of X-ray resistance and V(D)J recombination in mutant cells by Ku cDNA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Three genetic complementation groups of rodent cells are defective for both repair of x-ray-induced double-strand breaks and V(D)J recombination. Cells from one group lack a DNA end-binding activity that is biochemically and antigenically similar to the Ku autoantigen. Transfection of complementary DNA (cDNA) that encoded the 86-kilodalton subunit of Ku rescued these mutant cells for DNA end-binding activity, x-ray resistance, and V(D)J recombination activity. These results establish a role for Ku in DNA repair and recombination. Furthermore, as a component of a DNA-dependent protein kinase, Ku may initiate a signaling pathway induced by DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smider, V -- Rathmell, W K -- Lieber, M R -- Chu, G -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Nuclear ; Cell Line ; Cell Line, Transformed ; Cell Survival/*radiation effects ; Cricetinae ; DNA/*metabolism ; *DNA Helicases ; *DNA Repair ; DNA, Complementary ; DNA-Binding Proteins/genetics/*physiology ; Gene Rearrangement ; Genetic Complementation Test ; Humans ; Nuclear Proteins/genetics/*physiology ; Radiation Tolerance ; *Recombination, Genetic ; Transfection
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  • 97
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    Interaction of the p53-regulated protein Gadd45 with proliferating cell nuclear antigen (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: GADD45 is a ubiquitously expressed mammalian gene that is induced by DNA damage and certain other stresses. Like another p53-regulated gene, p21WAF1/CIP1, whose product binds to cyclin-dependent kinases (Cdk's) and proliferating cell nuclear antigen (PCNA), GADD45 has been associated with growth suppression. Gadd45 was found to bind to PCNA, a normal component of Cdk complexes and a protein involved in DNA replication and repair. Gadd45 stimulated DNA excision repair in vitro and inhibited entry of cells into S phase. These results establish GADD45 as a link between the p53-dependent cell cycle checkpoint and DNA repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, M L -- Chen, I T -- Zhan, Q -- Bae, I -- Chen, C Y -- Gilmer, T M -- Kastan, M B -- O'Connor, P M -- Fornace, A J Jr -- ES05777/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1376-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973727" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/metabolism ; DNA/biosynthesis ; DNA Damage ; *DNA Repair ; *Genes, p53 ; Humans ; Intracellular Signaling Peptides and Proteins ; Proliferating Cell Nuclear Antigen/*metabolism ; Proteins/*metabolism/pharmacology ; Recombinant Proteins/metabolism/pharmacology ; S Phase/*drug effects ; Transfection ; Tumor Cells, Cultured
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  • 98
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    The Sverdlovsk anthrax outbreak of 1979 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: In April and May 1979, an unusual anthrax epidemic occurred in Sverdlovsk, Union of Soviet Socialist Republics. Soviet officials attributed it to consumption of contaminated meat. U.S. agencies attributed it to inhalation of spores accidentally released at a military microbiology facility in the city. Epidemiological data show that most victims worked or lived in a narrow zone extending from the military facility to the southern city limit. Farther south, livestock died of anthrax along the zone's extended axis. The zone paralleled the northerly wind that prevailed shortly before the outbreak. It is concluded that the escape of an aerosol of anthrax pathogen at the military facility caused the outbreak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meselson, M -- Guillemin, J -- Hugh-Jones, M -- Langmuir, A -- Popova, I -- Shelokov, A -- Yampolskaya, O -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1202-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aerosols ; Aged ; *Air Microbiology ; Animals ; Animals, Domestic ; Anthrax/*epidemiology/history/microbiology/transmission/veterinary ; *Bacillus anthracis/immunology ; Bacterial Vaccines ; Biological Warfare ; *Disease Outbreaks/veterinary ; Female ; History, 20th Century ; Humans ; Male ; Meteorological Concepts ; Middle Aged ; Retrospective Studies ; Spores, Bacterial ; USSR/epidemiology ; Wind
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Naturally occurring variation in bristle number and DNA polymorphisms at the scabrous locus of Drosophila melanogaster (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-09
    Description: The association between quantitative genetic variation in bristle number and molecular variation at a candidate neurogenic locus, scabrous, was examined in Drosophila melanogaster. Approximately 32 percent of the genetic variation in abdominal bristle number (21 percent for sternopleural bristle number) among 47 second chromosomes from a natural population was correlated with DNA sequence polymorphisms at this locus. Several polymorphic sites associated with large phenotypic effects occurred at intermediate frequency. Quantitative genetic variation in natural populations caused by alleles that have large effects at a few loci and that segregate at intermediate frequencies conflicts with the classical infinitesimal model of the genetic basis of quantitative variation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lai, C -- Lyman, R F -- Long, A D -- Langley, C H -- Mackay, T F -- GM45146/GM/NIGMS NIH HHS/ -- GM45344/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1697-702.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Population Biology, University of California at Davis 95616.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992053" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; DNA/genetics ; *Drosophila Proteins ; Drosophila melanogaster/anatomy & histology/*genetics ; Female ; *Genes, Insect ; *Genetic Variation ; *Glycoproteins ; Haplotypes ; Linkage Disequilibrium ; Male ; Molecular Sequence Data ; Phenotype ; *Polymorphism, Genetic ; Proteins/*genetics ; Restriction Mapping ; Sense Organs/anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Adenosine inhibition of mesopontine cholinergic neurons: implications for EEG arousal (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Increased discharge activity of mesopontine cholinergic neurons participates in the production of electroencephalographic (EEG) arousal; such arousal diminishes as a function of the duration of prior wakefulness or of brain hyperthermia. Whole-cell and extracellular recordings in a brainstem slice show that mesopontine cholinergic neurons are under the tonic inhibitory control of endogenous adenosine, a neuromodulator released during brain metabolism. This inhibitory tone is mediated postsynaptically by an inwardly rectifying potassium conductance and by an inhibition of the hyperpolarization-activated current. These data provide a coupling mechanism linking neuronal control of EEG arousal with the effects of prior wakefulness, brain hyperthermia, and the use of the adenosine receptor blockers caffeine and theophylline.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612520/" 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/PMC3612520/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rainnie, D G -- Grunze, H C -- McCarley, R W -- Greene, R W -- R01 MH039683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Harvard University, Brockton, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303279" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*physiology ; Animals ; Arousal/*physiology ; Calcium/metabolism ; Electric Conductivity ; *Electroencephalography/drug effects ; Female ; Frontal Lobe/physiology ; In Vitro Techniques ; Male ; Membrane Potentials ; Neurons/*physiology ; Parasympathetic Nervous System/*physiology ; Potassium/metabolism ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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