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  • Articles  (178)
  • Male  (117)
  • Signal Transduction  (64)
  • American Association for the Advancement of Science (AAAS)  (178)
  • American Meteorological Society
  • American Physical Society (APS)
  • Springer Nature
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  • 1995-1999  (178)
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  • 1996  (178)
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  • Articles  (178)
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  • American Association for the Advancement of Science (AAAS)  (178)
  • American Meteorological Society
  • American Physical Society (APS)
  • Springer Nature
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  • 2010-2014
  • 2000-2004
  • 1995-1999  (178)
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  • 1
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Contraceptive technology. Panel wants to break R&D barrier (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1996 May 31;272(5266):1258.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650534" target="_blank"〉PubMed〈/a〉
    Keywords: *Contraceptive Agents/economics ; *Drug Industry/economics/legislation & jurisprudence ; Female ; Humans ; Institute of Medicine (U.S.) ; Insurance, Health ; Liability, Legal ; Male ; *Research/economics ; Research Support as Topic ; United States
    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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    Estimating the age of the common ancestor of men from the ZFY intron (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Y X -- Li, W H -- New York, N.Y. -- Science. 1996 May 31;272(5266):1356-7; author reply 1361-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bayes Theorem ; Biological Evolution ; Confidence Intervals ; DNA-Binding Proteins/*genetics ; *Genetics, Population ; Hominidae/*genetics ; Humans ; Introns/*genetics ; Kruppel-Like Transcription Factors ; Male ; Mutation ; Population Density ; Probability ; Time Factors ; Transcription Factors/*genetics ; Y Chromosome/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    HIV-1 Langerhans' cell tropism associated with heterosexual transmission of HIV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Heterosexual transmission by vaginal intercourse accounts for most transmission of human immunodeficiency virus-type 1 (HIV-1) in Africa and Asia but is less important in the HIV-1 epidemics of the United States and Western Europe. Epithelial Langerhans' cells (LCs) represent a possible source of initial cell contact for vaginal infection. Fifteen primary isolates of HIV-1 from U.S. homosexuals and 18 HIV-1 isolates from Thailand heterosexuals were evaluated for growth in LCs of U.S. origin. All the viruses from the Thai heterosexuals, which were subtype E, grew more efficiently in the LCs than any of the viruses from the U.S. homosexuals, which are subtype B. These results suggest that LC tropism is associated with the efficiency of heterosexual transmission of HIV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soto-Ramirez, L E -- Renjifo, B -- McLane, M F -- Marlink, R -- O'Hara, C -- Sutthent, R -- Wasi, C -- Vithayasai, P -- Vithayasai, V -- Apichartpiyakul, C -- Auewarakul, P -- Pena Cruz, V -- Chui, D S -- Osathanondh, R -- Mayer, K -- Lee, T H -- Essex, M -- 5 D43 TW0004/TW/FIC NIH HHS/ -- CA 39805/CA/NCI NIH HHS/ -- HL 33774/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard AIDS Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638113" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cells, Cultured ; HIV Core Protein p24/analysis ; HIV Infections/*transmission/virology ; HIV-1/classification/*growth & development/isolation & purification ; Homosexuality, Male ; Humans ; Langerhans Cells/*virology ; Macrophages/virology ; Male ; Monocytes/virology ; *Sexual Behavior ; Sexually Transmitted Diseases, Viral/*transmission/virology ; T-Lymphocytes/virology ; Thailand ; United States ; Virus Replication
    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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  • 5
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    Stimulation of membrane ruffling and MAP kinase activation by distinct effectors of RAS (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: The RAS guanine nucleotide binding proteins activate multiple signaling events that regulate cell growth and differentiation. In quiescent fibroblasts, ectopic expression of activated H-RAS (H-RASV12, where V12 indicates valine-12) induces membrane ruffling, mitogen-activated protein (MAP) kinase activation, and stimulation of DNA synthesis. A mutant of activated H-RAS, H-RASV12C40 (where C40 indicates cysteine-40), was identified that was defective for MAP kinase activation and stimulation of DNA synthesis, but retained the ability to induce membrane ruffling. Another mutant of activated H-RAS, H-RASV12S35 (where S35 indicates serine-35), which activates MAP kinase, was defective for stimulation of membrane ruffling and induction of DNA synthesis. Expression of both mutants resulted in a stimulation of DNA synthesis that was comparable to that induced by H-RASV12. These results indicate that membrane ruffling and activation of MAP kinase represent distinct RAS effector pathways and that input from both pathways is required for the mitogenic activity of RAS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- White, M A -- Wigler, M H -- Bar-Sagi, D -- CA 55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):810-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Division ; Cell Line ; Cell Membrane/*ultrastructure ; DNA/biosynthesis ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism ; Microinjections ; Mutation ; Plasmids ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Signal Transduction ; rac GTP-Binding Proteins ; ras Proteins/genetics/*metabolism
    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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    Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: Friedreich's ataxia (FRDA) is an autosomal recessive, degenerative disease that involves the central and peripheral nervous systems and the heart. A gene, X25, was identified in the critical region for the FRDA locus on chromosome 9q13. This gene encodes a 210-amino acid protein, frataxin, that has homologs in distant species such as Caenorhabditis elegans and yeast. A few FRDA patients were found to have point mutations in X25, but the majority were homozygous for an unstable GAA trinucleotide expansion in the first X25 intron.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Campuzano, V -- Montermini, L -- Molto, M D -- Pianese, L -- Cossee, M -- Cavalcanti, F -- Monros, E -- Rodius, F -- Duclos, F -- Monticelli, A -- Zara, F -- Canizares, J -- Koutnikova, H -- Bidichandani, S I -- Gellera, C -- Brice, A -- Trouillas, P -- De Michele, G -- Filla, A -- De Frutos, R -- Palau, F -- Patel, P I -- Di Donato, S -- Mandel, J L -- Cocozza, S -- Koenig, M -- Pandolfo, M -- 722/Telethon/Italy -- NS34192/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1423-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department de Genetica, University of Valencia, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596916" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Chromosomes, Human, Pair 9/*genetics ; DNA Primers ; Female ; Friedreich Ataxia/*genetics ; Genes, Recessive ; Heterozygote ; Humans ; *Introns ; *Iron-Binding Proteins ; Male ; Molecular Sequence Data ; Pedigree ; Point Mutation ; Polymerase Chain Reaction ; Proteins/chemistry/*genetics ; Sequence Alignment ; *Trinucleotide Repeats
    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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  • 7
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    Cooperative DNA binding and sequence-selective recognition conferred by the STAT amino-terminal domain (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: STAT proteins (signal transducers and activators of transcription) activate distinct target genes despite having similar DNA binding preferences. The transcriptional specificity of STAT proteins was investigated on natural STAT binding sites near the interferon-gamma gene. These sites are arranged in multiple copies and required cooperative interactions for STAT binding. The conserved amino-terminal domain of STAT proteins was required for cooperative DNA binding, although this domain was not essential for dimerization or binding to a single site. Cooperative binding interactions enabled the STAT proteins to recognize variations of the consensus site. These sites can be specific for the different STAT proteins and may function to direct selective transcriptional activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, X -- Sun, Y L -- Hoey, T -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):794-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Two Corporate Drive, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/immunology/*metabolism ; Interferon-gamma/genetics ; Introns ; Molecular Sequence Data ; Mutation ; Oligodeoxyribonucleotides/metabolism ; Promoter Regions, Genetic ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; Sequence Deletion ; Signal Transduction ; Trans-Activators/chemistry/immunology/*metabolism ; *Transcriptional Activation
    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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    Resistance to Leishmania major induced by tolerance to a single antigen (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: In mice, susceptibility to Leishmania major is associated with the early expansion of T helper 2 cells (TH2) cells, but nothing is known of the specificity of these cells. A previously identified antigen, Leishmania homolog of receptors for activated C kinase (LACK), was found to be the focus of this initial response. Mice made tolerant to LACK by the transgenic expression of the antigen in the thymus exhibited both a diminished TH2 response and a healing phenotype. Thus, T cells that are activated early and are reactive to a single antigen play a pivotal role in directing the immune response to the entire parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Julia, V -- Rassoulzadegan, M -- Glaichenhaus, N -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):421-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, Institut de Pharmacologie Moleculaire et Cellulaire, 660 Route des Lucioles, 06560 Valbonne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8832890" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/*immunology ; Crosses, Genetic ; Female ; Immune Tolerance ; Immunity, Innate ; Immunization ; Interleukin-4/secretion ; Interleukin-5/secretion ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Molecular Sequence Data ; Phenotype ; Protozoan Proteins/*immunology ; Th1 Cells/immunology ; Th2 Cells/*immunology
    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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  • 9
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    Intestinal secretory defects and dwarfism in mice lacking cGMP-dependent protein kinase II (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Cyclic guanosine 3',5'-monophosphate (cGMP)-dependent protein kinases (cGKs) mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK were resistant to Escherichia coli STa, an enterotoxin that stimulates cGMP accumulation and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was caused by a severe defect in endochondral ossification at the growth plates. These results indicate that cGKII plays a central role in diverse physiological processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeifer, A -- Aszodi, A -- Seidler, U -- Ruth, P -- Hofmann, F -- Fassler, R -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2082-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut f-ur Pharmakologie und Toxikologie, Technische Universitat Munchen, Biedersteiner Strasse 29, D-80802 M-unchen, Germany. pfeifer@ipt.med.tu-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953039" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Bacterial Toxins/toxicity ; Body Water/secretion ; *Bone Development ; Crosses, Genetic ; Cyclic GMP/analogs & derivatives/metabolism/pharmacology ; Cyclic GMP-Dependent Protein Kinases/deficiency/genetics/*metabolism ; Diarrhea/physiopathology ; Dwarfism/*enzymology/genetics/pathology ; Enterotoxins/toxicity ; Escherichia coli Proteins ; Female ; Gene Deletion ; Growth Plate/enzymology/pathology ; Intestinal Mucosa/*secretion ; Male ; Mice ; Mice, Inbred C57BL ; Osteogenesis ; Signal Transduction
    Print ISSN: 0036-8075
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  • 10
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    Brain activation modulated by sentence comprehension (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-04
    Description: The comprehension of visually presented sentences produces brain activation that increases with the linguistic complexity of the sentence. The volume of neural tissue activated (number of voxels) during sentence comprehension was measured with echo-planar functional magnetic resonance imaging. The modulation of the volume of activation by sentence complexity was observed in a network of four areas: the classical left-hemisphere language areas (the left laterosuperior temporal cortex, or Wernicke's area, and the left inferior frontal gyrus, or Broca's area) and their homologous right-hemisphere areas, although the right areas had much smaller volumes of activation than did the left areas. These findings generally indicate that the amount of neural activity that a given cognitive process engenders is dependent on the computational demand that the task imposes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Just, M A -- Carpenter, P A -- Keller, T A -- Eddy, W F -- Thulborn, K R -- MH-00662/MH/NIMH NIH HHS/ -- MH-19102/MH/NIMH NIH HHS/ -- MH-29617/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1996 Oct 4;274(5284):114-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Carnegie Mellon University, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8810246" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; *Brain Mapping ; Cognition/*physiology ; Dominance, Cerebral ; Female ; Frontal Lobe/anatomy & histology/*physiology ; Humans ; Language Tests ; Magnetic Resonance Imaging ; Male ; Temporal Lobe/anatomy & histology/*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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