ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
  • 1
    facet.materialart.
    Unbekannt
    Sequence interpretation. Functional annotation of mouse genome sequences (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2001-03-10
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nadeau, J H -- Balling, R -- Barsh, G -- Beier, D -- Brown, S D -- Bucan, M -- Camper, S -- Carlson, G -- Copeland, N -- Eppig, J -- Fletcher, C -- Frankel, W N -- Ganten, D -- Goldowitz, D -- Goodnow, C -- Guenet, J L -- Hicks, G -- Hrabe de Angelis, M -- Jackson, I -- Jacob, H J -- Jenkins, N -- Johnson, D -- Justice, M -- Kay, S -- Kingsley, D -- Lehrach, H -- Magnuson, T -- Meisler, M -- Poustka, A -- Rinchik, E M -- Rossant, J -- Russell, L B -- Schimenti, J -- Shiroishi, T -- Skarnes, W C -- Soriano, P -- Stanford, W -- Takahashi, J S -- Wurst, W -- Zimmer, A -- International Mouse Mutagenesis Consortium -- New York, N.Y. -- Science. 2001 Feb 16;291(5507):1251-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, BRB 624, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA. jhn4@po.cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11233449" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chromosome Mapping ; *Computational Biology ; Costs and Cost Analysis ; Genes/physiology ; Genetic Techniques ; *Genome ; *Genomics ; International Cooperation ; Mice/*genetics ; Mutagenesis ; Mutation ; Phenotype ; Private Sector ; Public Sector ; Research Support as Topic ; *Sequence Analysis, DNA
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 2
    facet.materialart.
    Unbekannt
    Role of the CLOCK protein in the mammalian circadian mechanism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1998-06-11
    Beschreibung: The mouse Clock gene encodes a bHLH-PAS protein that regulates circadian rhythms and is related to transcription factors that act as heterodimers. Potential partners of CLOCK were isolated in a two-hybrid screen, and one, BMAL1, was coexpressed with CLOCK and PER1 at known circadian clock sites in brain and retina. CLOCK-BMAL1 heterodimers activated transcription from E-box elements, a type of transcription factor-binding site, found adjacent to the mouse per1 gene and from an identical E-box known to be important for per gene expression in Drosophila. Mutant CLOCK from the dominant-negative Clock allele and BMAL1 formed heterodimers that bound DNA but failed to activate transcription. Thus, CLOCK-BMAL1 heterodimers appear to drive the positive component of per transcriptional oscillations, which are thought to underlie circadian rhythmicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gekakis, N -- Staknis, D -- Nguyen, H B -- Davis, F C -- Wilsbacher, L D -- King, D P -- Takahashi, J S -- Weitz, C J -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1564-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston MA 02115, USA. 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616112" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/genetics/*physiology ; Cloning, Molecular ; Cricetinae ; DNA/metabolism ; Dimerization ; Feedback ; Gene Expression ; Helix-Loop-Helix Motifs ; Male ; Mesocricetus ; Mice ; Mutation ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; Retina/metabolism ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; *Transcriptional Activation
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 3
    facet.materialart.
    Unbekannt
    Positional syntenic cloning and functional characterization of the mammalian circadian mutation tau (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-04-25
    Beschreibung: The tau mutation is a semidominant autosomal allele that dramatically shortens period length of circadian rhythms in Syrian hamsters. We report the molecular identification of the tau locus using genetically directed representational difference analysis to define a region of conserved synteny in hamsters with both the mouse and human genomes. The tau locus is encoded by casein kinase I epsilon (CKIepsilon), a homolog of the Drosophila circadian gene double-time. In vitro expression and functional studies of wild-type and tau mutant CKIepsilon enzyme reveal that the mutant enzyme has a markedly reduced maximal velocity and autophosphorylation state. In addition, in vitro CKIepsilon can interact with mammalian PERIOD proteins, and the mutant enzyme is deficient in its ability to phosphorylate PERIOD. We conclude that tau is an allele of hamster CKIepsilon and propose a mechanism by which the mutation leads to the observed aberrant circadian phenotype in mutant animals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869379/" 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/PMC3869379/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowrey, P L -- Shimomura, K -- Antoch, M P -- Yamazaki, S -- Zemenides, P D -- Ralph, M R -- Menaker, M -- Takahashi, J S -- R01MH56647/MH/NIMH NIH HHS/ -- R37MH39592/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):483-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Howard Hughes Medical Institute, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775102" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Casein Kinases ; Cell Cycle Proteins ; Chromosome Mapping ; *Circadian Rhythm/genetics ; Cloning, Molecular ; Cricetinae ; Female ; Heterozygote ; Humans ; Male ; Mesocricetus ; Mice ; Microsatellite Repeats ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Phenotype ; Phosphorylation ; *Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Protein Kinases/chemistry/*genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Suprachiasmatic Nucleus/metabolism
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 4
    facet.materialart.
    Unbekannt
    Role of mouse cryptochrome blue-light photoreceptor in circadian photoresponses (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1998-11-20
    Beschreibung: Cryptochromes are photoactive pigments in the eye that have been proposed to function as circadian photopigments. Mice lacking the cryptochrome 2 blue-light photoreceptor gene (mCry2) were tested for circadian clock-related functions. The mutant mice had a lower sensitivity to acute light induction of mPer1 in the suprachiasmatic nucleus (SCN) but exhibited normal circadian oscillations of mPer1 and mCry1 messenger RNA in the SCN. Behaviorally, the mutants had an intrinsic circadian period about 1 hour longer than normal and exhibited high-amplitude phase shifts in response to light pulses administered at circadian time 17. These data are consistent with the hypothesis that CRY2 protein modulates circadian responses in mice and suggest that cryptochromes have a role in circadian photoreception in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thresher, R J -- Vitaterna, M H -- Miyamoto, Y -- Kazantsev, A -- Hsu, D S -- Petit, C -- Selby, C P -- Dawut, L -- Smithies, O -- Takahashi, J S -- Sancar, A -- GM20069/GM/NIGMS NIH HHS/ -- GM31082/GM/NIGMS NIH HHS/ -- P0 AG11412/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1490-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9822380" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; *Drosophila Proteins ; *Eye Proteins ; Female ; Flavoproteins/genetics/*physiology ; Gene Expression Regulation ; Gene Targeting ; In Situ Hybridization ; *Light ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Mutation ; Nuclear Proteins/genetics ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Photoreceptor Cells, Vertebrate/*physiology ; Receptors, G-Protein-Coupled ; Suprachiasmatic Nucleus/metabolism
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 5
    facet.materialart.
    Unbekannt
    C57BL/6N mutation in cytoplasmic FMRP interacting protein 2 regulates cocaine response (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2013-12-21
    Beschreibung: The inbred mouse C57BL/6J is the reference strain for genome sequence and for most behavioral and physiological phenotypes. However, the International Knockout Mouse Consortium uses an embryonic stem cell line derived from a related C57BL/6N substrain. We found that C57BL/6N has a lower acute and sensitized response to cocaine and methamphetamine. We mapped a single causative locus and identified a nonsynonymous mutation of serine to phenylalanine (S968F) in Cytoplasmic FMRP interacting protein 2 (Cyfip2) as the causative variant. The S968F mutation destabilizes CYFIP2, and deletion of the C57BL/6N mutant allele leads to acute and sensitized cocaine-response phenotypes. We propose that CYFIP2 is a key regulator of cocaine response in mammals and present a framework to use mouse substrains to identify previously unknown genes and alleles regulating behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500108/" 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/PMC4500108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Vivek -- Kim, Kyungin -- Joseph, Chryshanthi -- Kourrich, Said -- Yoo, Seung-Hee -- Huang, Hung Chung -- Vitaterna, Martha H -- de Villena, Fernando Pardo-Manuel -- Churchill, Gary -- Bonci, Antonello -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- F32DA024556/DA/NIDA NIH HHS/ -- U01 MH061915/MH/NIMH NIH HHS/ -- U01MH61915/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 20;342(6165):1508-12. doi: 10.1126/science.1245503.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357318" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Substitution ; Animals ; Central Nervous System Stimulants/administration & dosage ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*genetics/*psychology ; *Drug-Seeking Behavior ; Methamphetamine/administration & dosage ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Mutation ; Nerve Tissue Proteins/genetics/*physiology ; Phenylalanine/genetics ; Polymorphism, Single Nucleotide ; Psychomotor Performance/drug effects ; Quantitative Trait Loci ; Serine/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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 6
    facet.materialart.
    Unbekannt
    Obesity and metabolic syndrome in circadian Clock mutant mice (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2005-04-23
    Beschreibung: The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764501/" 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/PMC3764501/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turek, Fred W -- Joshu, Corinne -- Kohsaka, Akira -- Lin, Emily -- Ivanova, Ganka -- McDearmon, Erin -- Laposky, Aaron -- Losee-Olson, Sue -- Easton, Amy -- Jensen, Dalan R -- Eckel, Robert H -- Takahashi, Joseph S -- Bass, Joseph -- AG11412/AG/NIA NIH HHS/ -- AG18200/AG/NIA NIH HHS/ -- DK02675/DK/NIDDK NIH HHS/ -- DK26356/DK/NIDDK NIH HHS/ -- HL59598/HL/NHLBI NIH HHS/ -- HL75029/HL/NHLBI NIH HHS/ -- K08 DK002675/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- R01 AG018200/AG/NIA NIH HHS/ -- R01 DK026356/DK/NIDDK NIH HHS/ -- R01 HL059598/HL/NHLBI NIH HHS/ -- R01 HL075029/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2005 May 13;308(5724):1043-5. Epub 2005 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845877" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipocytes/pathology ; Animals ; Body Weight ; Brain/metabolism ; CLOCK Proteins ; *Circadian Rhythm ; Dietary Fats/administration & dosage ; Energy Intake ; *Energy Metabolism ; *Feeding Behavior ; Hepatocytes/pathology ; Hyperglycemia ; Hyperlipidemias ; Insulin/blood ; Leptin/blood ; Metabolic Syndrome X/genetics/*physiopathology ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Mutation ; Neuropeptides/genetics/metabolism ; Obesity/genetics/*physiopathology ; Trans-Activators/*genetics/*physiology ; Weight Gain
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 7
    facet.materialart.
    Unbekannt
    Mutagenesis and mapping of a mouse gene, Clock, essential for circadian behavior (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-04-29
    Beschreibung: 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〉
    Schlagwort(e): Animals ; *Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Circadian Rhythm/*genetics ; Ethylnitrosourea ; Female ; *Genes ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; *Mutagenesis ; Phenotype
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 8
    facet.materialart.
    Unbekannt
    Forward and reverse genetic approaches to behavior in the mouse (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-06-17
    Beschreibung: 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〉
    Schlagwort(e): Animals ; *Behavior, Animal ; Circadian Rhythm/genetics ; Female ; *Genetic Techniques ; Genetics, Behavioral/*methods ; Learning ; Long-Term Potentiation ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mutagenesis
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 9
    facet.materialart.
    Unbekannt
    Circadian clock genes are ticking (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1992-10-09
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, J S -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):238-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NSF Center for Biological Timing, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1384127" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Circadian Rhythm/*genetics ; DNA/metabolism ; Drosophila/*genetics ; Drosophila Proteins ; Mutation ; *Nuclear Proteins ; Period Circadian Proteins ; Proteins/*genetics/physiology ; RNA/metabolism
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 10
    facet.materialart.
    Unbekannt
    Searching for genes underlying behavior: lessons from circadian rhythms (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-11-08
    Beschreibung: The success of forward genetic (from phenotype to gene) approaches to uncover genes that drive the molecular mechanism of circadian clocks and control circadian behavior has been unprecedented. Links among genes, cells, neural circuits, and circadian behavior have been uncovered in the Drosophila and mammalian systems, demonstrating the feasibility of finding single genes that have major effects on behavior. Why was this approach so successful in the elucidation of circadian rhythms? This article explores the answers to this question and describes how the methods used successfully for identifying the molecular basis of circadian rhythms can be applied to other behaviors such as anxiety, addiction, and learning and memory.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3744585/" 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/PMC3744585/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, Joseph S -- Shimomura, Kazuhiro -- Kumar, Vivek -- F32 DA024556/DA/NIDA NIH HHS/ -- P50 MH074924/MH/NIMH NIH HHS/ -- R01 MH078024/MH/NIMH NIH HHS/ -- U01 MH061915/MH/NIMH NIH HHS/ -- U01 MH61915/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):909-12. doi: 10.1126/science.1158822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Northwestern University, Evanston, IL 60208, USA. j-takahashi@northwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988844" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anxiety/genetics ; Behavior/*physiology ; Behavior, Addictive/genetics ; Behavior, Animal/*physiology ; Biological Clocks/*genetics ; Circadian Rhythm/*genetics ; *Genes ; *Genetic Techniques ; Humans ; Learning ; Mice ; Mutation ; Phenotype ; Point Mutation ; Sequence Analysis, DNA
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...