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  • 1
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    Gene expression during the life cycle of Drosophila melanogaster (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-28
    Description: Molecular genetic studies of Drosophila melanogaster have led to profound advances in understanding the regulation of development. Here we report gene expression patterns for nearly one-third of all Drosophila genes during a complete time course of development. Mutations that eliminate eye or germline tissue were used to further analyze tissue-specific gene expression programs. These studies define major characteristics of the transcriptional programs that underlie the life cycle, compare development in males and females, and show that large-scale gene expression data collected from whole animals can be used to identify genes expressed in particular tissues and organs or genes involved in specific biological and biochemical processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arbeitman, Michelle N -- Furlong, Eileen E M -- Imam, Farhad -- Johnson, Eric -- Null, Brian H -- Baker, Bruce S -- Krasnow, Mark A -- Scott, Matthew P -- Davis, Ronald W -- White, Kevin P -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2002 Sep 27;297(5590):2270-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12351791" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cluster Analysis ; Drosophila Proteins/genetics/physiology ; Drosophila melanogaster/embryology/*genetics/*growth & development ; Embryo, Nonmammalian/physiology ; Female ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; *Genes, Insect ; Germ Cells/physiology ; Larva/genetics ; Life Cycle Stages/*genetics ; Male ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; Pupa/genetics ; RNA, Messenger/genetics/metabolism ; Sex Characteristics ; Transcription, Genetic
    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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    Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
    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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    Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-01-06
    Description: Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S T -- Benson, B G -- Bramson, H N -- Chapman, D E -- Dickerson, S H -- Dold, K M -- Eberwein, D J -- Edelstein, M -- Frye, S V -- Gampe Jr, R T -- Griffin, R J -- Harris, P A -- Hassell, A M -- Holmes, W D -- Hunter, R N -- Knick, V B -- Lackey, K -- Lovejoy, B -- Luzzio, M J -- Murray, D -- Parker, P -- Rocque, W J -- Shewchuk, L -- Veal, J M -- Walker, D H -- Kuyper, L F -- New York, N.Y. -- Science. 2001 Jan 5;291(5501):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Glaxo Wellcome Research and Development, Research Triangle Park, NC 27709, USA. std41085@glaxowellcome.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11141566" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*chemically induced/*prevention & control ; Animals ; Animals, Newborn ; Antineoplastic Agents/*toxicity ; Antineoplastic Combined Chemotherapy Protocols/toxicity ; Apoptosis/drug effects ; *CDC2-CDC28 Kinases ; Cell Cycle/drug effects ; Cell Line ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclophosphamide/toxicity ; Cytoprotection/drug effects ; DNA/biosynthesis ; Doxorubicin/toxicity ; Drug Design ; Enzyme Inhibitors/chemical synthesis/chemistry/*pharmacology ; Epithelium/drug effects ; Etoposide/toxicity ; Hair Follicle/cytology/*drug effects ; Humans ; Indoles/chemical synthesis/chemistry/*pharmacology ; Mice ; Mice, SCID ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Rats ; Retinoblastoma Protein/metabolism ; Scalp/transplantation ; Sulfonamides/chemical synthesis/chemistry/*pharmacology ; Transplantation, Heterologous
    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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    Role of the guanosine triphosphatase Rac2 in T helper 1 cell differentiation (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-24
    Description: T helper 1 (TH1) cells mediate cellular immunity, whereas TH2 cells potentiate antiparasite and humoral immunity. We used a complementary DNA subtraction method, representational display analysis, to show that the small guanosine triphosphatase Rac2 is expressed selectively in murine TH1 cells. Rac induces the interferon-gamma (IFN-gamma) promoter through cooperative activation of the nuclear factor kappa B and p38 mitogen-activated protein kinase pathways. Tetracycline-regulated transgenic mice expressing constitutively active Rac2 in T cells exhibited enhanced IFN-gamma production. Dominant-negative Rac inhibited IFN-gamma production in murine T cells. Moreover, T cells from Rac2-/- mice showed decreased IFN-gamma production under TH1 conditions in vitro. Thus, Rac2 activates TH1-specific signaling and IFN-gamma gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, B -- Yu, H -- Zheng, W -- Voll, R -- Na, S -- Roberts, A W -- Williams, D A -- Davis, R J -- Ghosh, S -- Flavell, R A -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2219-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06520-8011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864872" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cells, Cultured ; Cytokines/biosynthesis/genetics ; Gene Expression Regulation ; Humans ; Interferon-gamma/biosynthesis/*genetics ; JNK Mitogen-Activated Protein Kinases ; Jurkat Cells ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Promoter Regions, Genetic ; Signal Transduction ; Th1 Cells/cytology/*immunology/*metabolism ; Transfection ; p38 Mitogen-Activated Protein Kinases ; rac GTP-Binding 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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  • 5
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    Gamma oscillations and object processing in the infant brain (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: An enduring controversy in neuroscience concerns how the brain "binds" together separately coded stimulus features to form unitary representations of objects. Recent evidence has indicated a close link between this binding process and 40-hertz (gamma-band) oscillations generated by localized neural circuits. In a separate line of research, the ability of young infants to perceive objects as unitary and bounded has become a central focus for debates about the mechanisms of perceptual development. Here we demonstrate that binding-related 40-hertz oscillations are evident in the infant brain around 8 months of age, which is the same age at which behavioral and event-related potential evidence indicates the onset of perceptual binding of spatially separated static visual features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Csibra, G -- Davis, G -- Spratling, M W -- Johnson, M H -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Brain and Cognitive Development, School of Psychology, Birkbeck College, University of London, Malet Street, London WC1E 7HX, UK. g.csibra@bbk.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090357" target="_blank"〉PubMed〈/a〉
    Keywords: *Electroencephalography ; Evoked Potentials, Visual ; Female ; *Form Perception ; Frontal Lobe/*physiology ; Humans ; Infant ; Male ; Occipital Lobe/physiology ; Parietal Lobe/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Role of apoptosis in Pseudomonas aeruginosa pneumonia (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-12-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotchkiss, R S -- Dunne, W M -- Swanson, P E -- Davis, C G -- Tinsley, K W -- Chang, K C -- Buchman, T G -- Karl, I E -- GM44118/GM/NIGMS NIH HHS/ -- GM55194/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Nov 30;294(5548):1783.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, Washington University School of Medicine, 660 South Euclid, St. Louis, MO 63110, USA. hotch@morpheus.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11729269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/genetics/metabolism ; *Apoptosis ; Bronchi/enzymology/metabolism/pathology/ultrastructure ; Caspase 3 ; Caspases/metabolism ; Chromatin/metabolism/pathology/ultrastructure ; DNA, Single-Stranded/analysis ; Endothelium, Vascular/enzymology/metabolism/pathology ; Epithelial Cells/enzymology/metabolism/pathology/ultrastructure ; False Positive Reactions ; Gene Deletion ; In Situ Nick-End Labeling ; Lymphocytes/enzymology/metabolism/pathology ; Mice ; Microscopy, Electron ; Pneumonia, Bacterial/enzymology/metabolism/*pathology ; Pseudomonas Infections/enzymology/metabolism/*pathology ; Pseudomonas aeruginosa/*physiology ; Reproducibility of Results ; Sepsis/enzymology/metabolism/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Regulation of daily locomotor activity and sleep by hypothalamic EGF receptor signaling (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-12-26
    Description: The circadian clock in the suprachiasmatic nucleus (SCN) is thought to drive daily rhythms of behavior by secreting factors that act locally within the hypothalamus. In a systematic screen, we identified transforming growth factor-alpha (TGF-alpha) as a likely SCN inhibitor of locomotion. TGF-alpha is expressed rhythmically in the SCN, and when infused into the third ventricle it reversibly inhibited locomotor activity and disrupted circadian sleep-wake cycles. These actions are mediated by epidermal growth factor (EGF) receptors on neurons in the hypothalamic subparaventricular zone. Mice with a hypomorphic EGF receptor mutation exhibited excessive daytime locomotor activity and failed to suppress activity when exposed to light. These results implicate EGF receptor signaling in the daily control of locomotor activity, and identify a neural circuit in the hypothalamus that likely mediates the regulation of behavior both by the SCN and the retina.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kramer, A -- Yang, F C -- Snodgrass, P -- Li, X -- Scammell, T E -- Davis, F C -- Weitz, C J -- HD-18686/HD/NICHD NIH HHS/ -- MH62589/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2511-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11752569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/drug effects/physiology ; Body Temperature/drug effects ; Cerebral Ventricles/metabolism ; Circadian Rhythm/drug effects/*physiology ; Cricetinae ; Darkness ; Epidermal Growth Factor/pharmacology ; Female ; Hypothalamus/*metabolism ; Ligands ; Light ; Male ; Mesocricetus ; Mice ; *Motor Activity/drug effects ; Neural Pathways/physiology ; Neurons/metabolism ; Point Mutation ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Retina/metabolism ; Retinal Ganglion Cells/metabolism ; Signal Transduction ; Sleep/drug effects/*physiology ; Suprachiasmatic Nucleus/*metabolism ; Transforming Growth Factor alpha/administration & ; dosage/genetics/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Immunology. The immunological synapse--a multitasking system (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Der Merwe, P Anton -- Davis, Simon J -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1479-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. anton.vandermerwe@path.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859183" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigen-Presenting Cells/*immunology ; Antigens, CD ; Antigens, CD28/immunology/metabolism ; Antigens, CD80/immunology/metabolism ; Antigens, Differentiation/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen ; Dimerization ; Histocompatibility Antigens Class II/metabolism ; *Immunoconjugates ; Immunoglobulin alpha-Chains/immunology/metabolism ; Intercellular Junctions/*immunology ; Ligands ; Lipid Bilayers ; Lymphocyte Activation ; Mice ; Peptides/immunology/metabolism ; Receptor Aggregation ; Receptors, Antigen, T-Cell/*immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; Time Factors
    Print ISSN: 0036-8075
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  • 9
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    Beta-arrestin 2: a receptor-regulated MAPK scaffold for the activation of JNK3 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: beta-Arrestins, originally discovered in the context of heterotrimeric guanine nucleotide binding protein-coupled receptor (GPCR) desensitization, also function in internalization and signaling of these receptors. We identified c-Jun amino-terminal kinase 3 (JNK3) as a binding partner of beta-arrestin 2 using a yeast two-hybrid screen and by coimmunoprecipitation from mouse brain extracts or cotransfected COS-7 cells. The upstream JNK activators apoptosis signal-regulating kinase 1 (ASK1) and mitogen-activated protein kinase (MAPK) kinase 4 were also found in complex with beta-arrestin 2. Cellular transfection of beta-arrestin 2 caused cytosolic retention of JNK3 and enhanced JNK3 phosphorylation stimulated by ASK1. Moreover, stimulation of the angiotensin II type 1A receptor activated JNK3 and triggered the colocalization of beta-arrestin 2 and active JNK3 to intracellular vesicles. Thus, beta-arrestin 2 acts as a scaffold protein, which brings the spatial distribution and activity of this MAPK module under the control of a GPCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, P H -- Chow, C W -- Miller, W E -- Laporte, S A -- Field, M E -- Lin, F T -- Davis, R J -- Lefkowitz, R J -- CA65861/CA/NCI NIH HHS/ -- CA85422/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Box 3821, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090355" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; COS Cells ; Cell Line ; Cell Nucleus/metabolism ; Cytosol/enzymology/metabolism ; Endosomes/enzymology/metabolism ; Enzyme Activation ; Humans ; *MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinase 5 ; MAP Kinase Kinase Kinases/*metabolism ; *MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 10 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Rats ; Receptor, Angiotensin, Type 1 ; Receptors, Angiotensin/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Two-Hybrid System Techniques
    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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  • 10
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    Protein kinase C overactivity impairs prefrontal cortical regulation of working memory (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-30
    Description: The prefrontal cortex is a higher brain region that regulates thought, behavior, and emotion using representational knowledge, operations often referred to as working memory. We tested the influence of protein kinase C (PKC) intracellular signaling on prefrontal cortical cognitive function and showed that high levels of PKC activity in prefrontal cortex, as seen for example during stress exposure, markedly impair behavioral and electrophysiological measures of working memory. These data suggest that excessive PKC activation can disrupt prefrontal cortical regulation of behavior and thought, possibly contributing to signs of prefrontal cortical dysfunction such as distractibility, impaired judgment, impulsivity, and thought disorder.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birnbaum, S G -- Yuan, P X -- Wang, M -- Vijayraghavan, S -- Bloom, A K -- Davis, D J -- Gobeske, K T -- Sweatt, J D -- Manji, H K -- Arnsten, A F T -- AG06036/AG/NIA NIH HHS/ -- P50 MH068789/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):882-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale Medical School, 333 Cedar Street, New Haven, CT 06520-8001, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514161" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Alkaloids ; Animals ; Benzophenanthridines ; Carbolines/pharmacology ; Electrophysiology ; Enzyme Activation ; Female ; Imidazoles/pharmacology ; Lithium Carbonate/pharmacology ; Macaca mulatta ; Male ; Memory/drug effects/*physiology ; Neurons/drug effects/physiology ; Phenanthridines/pharmacology ; Prefrontal Cortex/enzymology/*physiology ; Protein Kinase C/antagonists & inhibitors/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, alpha-1/physiology ; Signal Transduction ; Stress, Physiological/physiopathology ; Tetradecanoylphorbol Acetate/pharmacology ; Valproic Acid/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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