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  • Cell Line  (3)
  • Mutation  (2)
  • Female
  • Models, Molecular
  • 2000-2004  (6)
  • 1
    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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  • 2
    Publication Date: 2002-07-20
    Description: Mammalian organogenesis requires the expansion of pluripotent precursor cells before the subsequent determination of specific cell types, but the tissue-specific molecular mechanisms that regulate the initial expansion of primordial cells remain poorly defined. We have genetically established that Six6 homeodomain factor, acting as a strong tissue-specific repressor, regulates early progenitor cell proliferation during mammalian retinogenesis and pituitary development. Six6, in association with Dach corepressors, regulates proliferation by directly repressing cyclin-dependent kinase inhibitors, including the p27Kip1 promoter. These data reveal a molecular mechanism by which a tissue-specific transcriptional repressor-corepressor complex can provide an organ-specific strategy for physiological expansion of precursor populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Xue -- Perissi, Valentina -- Liu, Forrest -- Rose, David W -- Rosenfeld, Michael G -- 484/B/Telethon/Italy -- 5F32DK09814/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 16;297(5584):1180-3. Epub 2002 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Medicine, University of California, San Diego, School of Medicine, 9500 Gilman Drive, Room 345, La Jolla, CA 92093-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12130660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle ; Cell Cycle Proteins/genetics/metabolism ; *Cell Division ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Embryo, Mammalian/cytology ; Eye Proteins/metabolism ; Homeodomain Proteins/*genetics/*metabolism ; Mice ; Nuclear Proteins/metabolism ; Organ Specificity ; Pituitary Gland/*cytology/embryology ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/metabolism ; Retina/*cytology/embryology ; Retinal Ganglion Cells/cytology/physiology ; Stem Cells/*physiology ; Trans-Activators/*genetics/*metabolism ; Transcription Factors ; Transcription, Genetic ; Transfection ; Tumor Suppressor Proteins/genetics/metabolism ; Up-Regulation
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-05-23
    Description: RNA silencing is a sequence-specific RNA degradation mechanism that is operational in plants and animals. Here, we show that flock house virus (FHV) is both an initiator and a target of RNA silencing in Drosophila host cells and that FHV infection requires suppression of RNA silencing by an FHV-encoded protein, B2. These findings establish RNA silencing as an adaptive antiviral defense in animal cells. B2 also inhibits RNA silencing in transgenic plants, providing evidence for a conserved RNA silencing pathway in the plant and animal kingdoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Hongwei -- Li, Wan Xiang -- Ding, Shou Wei -- New York, N.Y. -- Science. 2002 May 17;296(5571):1319-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology and Center for Plant Cell Biology, University of California, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016316" target="_blank"〉PubMed〈/a〉
    Keywords: Agrobacterium tumefaciens/genetics ; Animals ; Cell Line ; Drosophila/genetics/*virology ; *Gene Silencing ; Genes, Viral ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Nodaviridae/*genetics/*physiology ; Plant Leaves/genetics/metabolism ; Plants, Genetically Modified ; RNA, Double-Stranded/genetics/metabolism ; RNA, Small Interfering ; RNA, Untranslated/*metabolism ; RNA, Viral/genetics/metabolism ; Tobacco/*genetics/metabolism/microbiology ; Transfection ; Viral Proteins/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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  • 4
    Publication Date: 2004-12-25
    Description: beta-arrestins are multifunctional proteins that act as scaffolds and transducers of intracellular signals from heptahelical transmembrane-spanning receptors (7TMR). Hedgehog (Hh) signaling, which uses the putative 7TMR, Smoothened, is established as a fundamental pathway in development, and unregulated Hh signaling is associated with certain malignancies. Here, we show that the functional knockdown of beta-arrestin 2 in zebrafish embryos recapitulates the many phenotypes of Hh pathway mutants. Expression of wild-type beta-arrestin 2, or constitutive activation of the Hh pathway downstream of Smoothened, rescues the phenotypes caused by beta-arrestin 2 deficiency. These results suggest that a functional interaction between beta-arrestin 2 and Smoothened may be critical to regulate Hh signaling in zebrafish development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilbanks, Alyson M -- Fralish, Gregory B -- Kirby, Margaret L -- Barak, Larry S -- Li, Yin-Xiong -- Caron, Marc G -- GM069086-01/GM/NIGMS NIH HHS/ -- HL36059/HL/NHLBI NIH HHS/ -- HL61365/HL/NHLBI NIH HHS/ -- NS19576/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2264-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Center for Models of Human Disease, Institute for Genome Science and Policy, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15618520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*physiology ; Cell Differentiation ; Cyclic AMP-Dependent Protein Kinases/genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Gene Expression Regulation, Developmental ; Hedgehog Proteins ; Homeodomain Proteins/genetics/metabolism ; In Situ Hybridization ; Membrane Proteins/genetics/metabolism ; Muscle Cells/cytology ; Muscle Fibers, Skeletal/cytology ; Mutation ; Phenotype ; Receptors, Cell Surface ; Receptors, G-Protein-Coupled/genetics/physiology ; Repressor Proteins/genetics/metabolism ; *Signal Transduction ; Trans-Activators/genetics/*metabolism ; Transcription Factors/genetics/metabolism ; Zebrafish/*embryology/genetics/*metabolism ; Zebrafish Proteins/genetics/metabolism/*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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  • 5
    Publication Date: 2004-04-24
    Description: Parkin is an E3 ubiquitin ligase involved in the ubiquitination of proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD). We show that parkin is S-nitrosylated in vitro, as well as in vivo in a mouse model of PD and in brains of patients with PD and diffuse Lewy body disease. Moreover, S-nitrosylation inhibits parkin's ubiquitin E3 ligase activity and its protective function. The inhibition of parkin's ubiquitin E3 ligase activity by S-nitrosylation could contribute to the degenerative process in these disorders by impairing the ubiquitination of parkin substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Kenny K K -- Thomas, Bobby -- Li, Xiaojie -- Pletnikova, Olga -- Troncoso, Juan C -- Marsh, Laura -- Dawson, Valina L -- Dawson, Ted M -- NS38377/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 May 28;304(5675):1328-31. Epub 2004 Apr 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105460" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Carrier Proteins/genetics/metabolism ; Catalytic Domain ; Cell Death ; Cell Line ; Cysteine Proteinase Inhibitors/pharmacology ; Humans ; Lewy Body Disease/metabolism ; MPTP Poisoning/metabolism ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/genetics/metabolism ; Nitric Oxide/*metabolism ; Nitric Oxide Donors/pharmacology ; Nitric Oxide Synthase/genetics/metabolism ; Parkinson Disease/*metabolism ; Recombinant Proteins/metabolism ; Synucleins ; Transfection ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligases/antagonists & inhibitors/chemistry/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
    ISSN: 1435-232X
    Keywords: Key words Holocarboxylase synthetase ; Multiple carboxylase deficiency ; Biotin ; Mutation ; Microsatellite markers ; Haplotype
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Holocarboxylase synthetase (HCS) deficiency is a rare autosomal recessive disorder of biotin metabolism. Including three new Japanese patients we diagnosed in this study, ten Japanese families have, so far, been accumulated. In these families, the mutations 237Leu 〉 Pro (sevenalleles) and 1067delG (five alleles) were predominant; 508Arg 〉 Trp and 550Val 〉 Met mutations were identified in three families in the heterozygous form and in one patient in the homozygous form, respectively. To determine the origin of these mutations, we identified new polymorphic microsatellite markers in the HCS gene and analyzed the haplotypes of the patients. All the 237Leu 〉 Pro and the 1067delG alleles were associated with haplotype 2-2. This finding is consistent with the notion that these mutations are founder mutations in the Japanese population. Three Japanese 508Arg 〉 Trp alleles were associated with several haplotypes, including 2-3 and 1-4. The haplotype of a Taiwanese patient homozygous for the 508Arg 〉 Trp mutation was 2-3/2-3. The haplotype of one Japanese patient homozygous for the 550Val 〉 Met mutation was 1-4/1-4, whereas that of a Jewish patient with the same homozygous mutation was 2-3/2-3. Both mutations were associated with at least two haplotypes and were found in several ethnic groups. The changes 508Arg 〉 Trp and 550Val 〉 Met occurred at CpG dinucleotide. The data suggest that these two mutations represent a mutational hot-spot.
    Type of Medium: Electronic Resource
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