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  • Rats  (8)
  • American Association for the Advancement of Science (AAAS)  (8)
  • Cambridge University Press
  • Springer
  • 2005-2009  (1)
  • 2000-2004  (4)
  • 1980-1984  (3)
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  • 1
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    Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2001-01-06
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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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
    Publikationsdatum: 2000-11-25
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Knockout rats via embryo microinjection of zinc-finger nucleases (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2009-07-25
    Beschreibung: The toolbox of rat genetics currently lacks the ability to introduce site-directed, heritable mutations into the genome to create knockout animals. By using engineered zinc-finger nucleases (ZFNs) designed to target an integrated reporter and two endogenous rat genes, Immunoglobulin M (IgM) and Rab38, we demonstrate that a single injection of DNA or messenger RNA encoding ZFNs into the one-cell rat embryo leads to a high frequency of animals carrying 25 to 100% disruption at the target locus. These mutations are faithfully and efficiently transmitted through the germline. Our data demonstrate the feasibility of targeted gene disruption in multiple rat strains within 4 months time, paving the way to a humanized monoclonal antibody platform and additional human disease models.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831805/" 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/PMC2831805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geurts, Aron M -- Cost, Gregory J -- Freyvert, Yevgeniy -- Zeitler, Bryan -- Miller, Jeffrey C -- Choi, Vivian M -- Jenkins, Shirin S -- Wood, Adam -- Cui, Xiaoxia -- Meng, Xiangdong -- Vincent, Anna -- Lam, Stephen -- Michalkiewicz, Mieczyslaw -- Schilling, Rebecca -- Foeckler, Jamie -- Kalloway, Shawn -- Weiler, Hartmut -- Menoret, Severine -- Anegon, Ignacio -- Davis, Gregory D -- Zhang, Lei -- Rebar, Edward J -- Gregory, Philip D -- Urnov, Fyodor D -- Jacob, Howard J -- Buelow, Roland -- 5P01HL082798-03/HL/NHLBI NIH HHS/ -- 5U01HL066579-08/HL/NHLBI NIH HHS/ -- P01 HL082798/HL/NHLBI NIH HHS/ -- P01 HL082798-03/HL/NHLBI NIH HHS/ -- U01 HL066579/HL/NHLBI NIH HHS/ -- U01 HL066579-08/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):433. doi: 10.1126/science.1172447.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, WI 52336, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628861" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; Dna ; Embryo, Mammalian ; Endodeoxyribonucleases/genetics/*metabolism ; Feasibility Studies ; Female ; *Gene Knockout Techniques ; Green Fluorescent Proteins ; Immunoglobulin M/*genetics ; Male ; *Microinjections ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; RNA, Messenger ; Rats ; *Zinc Fingers/genetics ; rab GTP-Binding Proteins/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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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
    Publikationsdatum: 2004-10-30
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Niemann-Pick C1 Like 1 protein is critical for intestinal cholesterol absorption (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-02-21
    Beschreibung: Dietary cholesterol consumption and intestinal cholesterol absorption contribute to plasma cholesterol levels, a risk factor for coronary heart disease. The molecular mechanism of sterol uptake from the lumen of the small intestine is poorly defined. We show that Niemann-Pick C1 Like 1(NPC1L1) protein plays a critical role in the absorption of intestinal cholesterol. NPC1L1 expression is enriched in the small intestine and is in the brush border membrane of enterocytes. Although otherwise phenotypically normal, NPC1L1-deficient mice exhibit a substantial reduction in absorbed cholesterol, which is unaffected by dietary supplementation of bile acids. Ezetimibe, a drug that inhibits cholesterol absorption, had no effect in NPC1L1 knockout mice, suggesting that NPC1L1 resides in an ezetimibe-sensitive pathway responsible for intestinal cholesterol absorption.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altmann, Scott W -- Davis, Harry R Jr -- Zhu, Li-Ji -- Yao, Xiaorui -- Hoos, Lizbeth M -- Tetzloff, Glen -- Iyer, Sai Prasad N -- Maguire, Maureen -- Golovko, Andrei -- Zeng, Ming -- Wang, Luquan -- Murgolo, Nicholas -- Graziano, Michael P -- New York, N.Y. -- Science. 2004 Feb 20;303(5661):1201-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiovascular/Endocrine Research, Schering-Plough Research Institute, 2015 Galloping Hill Road, Kenilworth, NJ, 07033-0539, USA. scott.altmann@spcorp.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976318" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Anticholesteremic Agents/pharmacology ; Azetidines/pharmacology ; Cholesterol/*metabolism ; Cholesterol, Dietary/*metabolism ; Cholic Acid/administration & dosage/pharmacology ; Computational Biology ; Enterocytes/*metabolism ; Ezetimibe ; Female ; Gene Expression Profiling ; Humans ; *Intestinal Absorption/drug effects ; Intestine, Small/metabolism ; Jejunum/metabolism ; Liver/metabolism ; Male ; Membrane Proteins/chemistry/genetics/*metabolism ; Membrane Transport Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; Proteins/chemistry/genetics/*metabolism ; Rats ; Rats, Sprague-Dawley
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Excitatory and inhibitory effects of serotonin on sensorimotor reactivity measured with acoustic startle (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1980-07-25
    Beschreibung: Serotonin infused into the lateral ventricle in rats produced a dose-dependent depression of the acoustic startle reflex. When infused onto the spinal cord, serotonin produced a dose-dependent increase in startle. Thus the same neurotransmitter can modulate the same behavior in opposite ways, depending on which part of the central nervous system is involved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, M -- Strachan, D I -- Kass, E -- New York, N.Y. -- Science. 1980 Jul 25;209(4455):521-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7394520" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Dose-Response Relationship, Drug ; Kinetics ; Male ; Rats ; Reflex, Acoustic/*drug effects ; Reflex, Startle/*drug effects ; Serotonin/*pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Habituation and sensitization of startle reflexes elicited electrically from the brainstem (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1982-11-12
    Beschreibung: Repetitive elicitation of startle-like responses by electrical stimulation of the cochlear nucleus led to sensitization followed by habituation. In contrast, repetitive elicitation of startle-like responses by electrical stimulation of the reticular formation led only to sensitization. Since these different locations represent different points along the acoustic startle circuit, the data suggest that sensitization may be related to the motor side of reflex arcs, whereas habituation may be related to the sensory side.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, M -- Parisi, T -- Gendelman, D S -- Tischler, M -- Kehne, J H -- MH-00004/MH/NIMH NIH HHS/ -- MH-18949/MH/NIMH NIH HHS/ -- MH-25642/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1982 Nov 12;218(4573):688-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7134967" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Auditory Pathways/*physiology ; Brain Stem/*physiology ; Cochlear Nerve/physiology ; *Habituation, Psychophysiologic ; Male ; Rats ; Reflex ; Reflex, Startle/*physiology ; Sound
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Sustained intracerebroventricular infusion of brain fuels reduces body weight and food intake in rats (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1981-04-03
    Beschreibung: Long-term infusion of glucose, beta-hydroxybutyrate, and glycerol into the third ventricle of the rat brain caused a stabilization of body weight at a lower than normal level. Among the glucose- and glycerol-treated animals this weight loss was caused in part by temporary hypophagia. Among the animals treated with beta-hydroxybutyrate the weight loss was unaccompanied by a reduction in food intake. The results are consistent with the view that the systems controlling food intake and body weight are sensitive to the availability of brain fuels. They are not consistent however, with the view that these control systems monitor calories independently of their source.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, J D -- Wirtshafter, D -- Asin, K E -- Brief, D -- AM 26030/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):81-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7193909" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3-Hydroxybutyric Acid ; Animals ; *Appetite Regulation/drug effects ; *Body Weight/drug effects ; Brain/drug effects/*physiology ; Circadian Rhythm ; Drinking/drug effects ; *Eating/drug effects ; Glucose/*pharmacology ; Glycerol/*pharmacology ; Hydroxybutyrates/administration & dosage/*pharmacology ; Hypothalamus/drug effects ; Injections, Intraventricular ; Male ; Rats
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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