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  • Animals, Genetically Modified  (2)
  • Darkness  (2)
  • Gene Expression Regulation  (2)
  • 1
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    Entrainment of the circadian clock in the liver by feeding (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-13
    Description: Circadian rhythms of behavior are driven by oscillators in the brain that are coupled to the environmental light cycle. Circadian rhythms of gene expression occur widely in peripheral organs. It is unclear how these multiple rhythms are coupled together to form a coherent system. To study such coupling, we investigated the effects of cycles of food availability (which exert powerful entraining effects on behavior) on the rhythms of gene expression in the liver, lung, and suprachiasmatic nucleus (SCN). We used a transgenic rat model whose tissues express luciferase in vitro. Although rhythmicity in the SCN remained phase-locked to the light-dark cycle, restricted feeding rapidly entrained the liver, shifting its rhythm by 10 hours within 2 days. Our results demonstrate that feeding cycles can entrain the liver independently of the SCN and the light cycle, and they suggest the need to reexamine the mammalian circadian hierarchy. They also raise the possibility that peripheral circadian oscillators like those in the liver may be coupled to the SCN primarily through rhythmic behavior, such as feeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokkan, K A -- Yamazaki, S -- Tei, H -- Sakaki, Y -- Menaker, M -- MH 56647/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2001 Jan 19;291(5503):490-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Science Foundation Center for Biological Timing and Department of Biology, University of Virginia, P.O. Box 400328, Charlottesville, VA 22904-4328, USA. mm7e@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11161204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Circadian Rhythm ; Corticosterone/blood/pharmacology ; Culture Techniques ; Eating ; Female ; *Food ; *Gene Expression Regulation ; Genes, Reporter ; Liver/*physiology ; Luciferases/genetics ; Lung/physiology ; Male ; Motor Activity ; Organ Specificity ; Rats ; Suprachiasmatic Nucleus/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Resetting central and peripheral circadian oscillators in transgenic rats (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-28
    Description: In multicellular organisms, circadian oscillators are organized into multitissue systems which function as biological clocks that regulate the activities of the organism in relation to environmental cycles and provide an internal temporal framework. To investigate the organization of a mammalian circadian system, we constructed a transgenic rat line in which luciferase is rhythmically expressed under the control of the mouse Per1 promoter. Light emission from cultured suprachiasmatic nuclei (SCN) of these rats was invariably and robustly rhythmic and persisted for up to 32 days in vitro. Liver, lung, and skeletal muscle also expressed circadian rhythms, which damped after two to seven cycles in vitro. In response to advances and delays of the environmental light cycle, the circadian rhythm of light emission from the SCN shifted more rapidly than did the rhythm of locomotor behavior or the rhythms in peripheral tissues. We hypothesize that a self-sustained circadian pacemaker in the SCN entrains circadian oscillators in the periphery to maintain adaptive phase control, which is temporarily lost following large, abrupt shifts in the environmental light cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamazaki, S -- Numano, R -- Abe, M -- Hida, A -- Takahashi, R -- Ueda, M -- Block, G D -- Sakaki, Y -- Menaker, M -- Tei, H -- MH56647/MH/NIMH NIH HHS/ -- R01 MH056647/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 28;288(5466):682-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NSF Center for Biological Timing and Department of Biology, University of Virginia, Charlottesville, VA 22903-2477, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10784453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Biological Clocks/*physiology ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Culture Techniques ; Darkness ; Genes, Reporter ; Light ; Liver/physiology ; Luciferases/genetics/metabolism ; Lung/physiology ; Male ; Mice ; Motor Activity ; Muscle, Skeletal/physiology ; Nuclear Proteins/genetics/physiology ; Period Circadian Proteins ; Promoter Regions, Genetic ; Rats ; Suprachiasmatic Nucleus/*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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  • 3
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    Comment on "Differential rescue of light- and food-entrainable circadian rhythms" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-01
    Description: Fuller et al. (Reports, 23 May 2008, p. 1074) reported that the dorsomedial hypothalamus contains a Bmal1-based oscillator that can drive food-entrained circadian rhythms. We report that mice bearing a null mutation of Bmal1 exhibit normal food-anticipatory circadian rhythms. Lack of food anticipation in Bmal1-/- mice reported by Fuller et al. may reflect morbidity due to weight loss, thus raising questions about their conclusions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583785/" 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/PMC2583785/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mistlberger, Ralph E -- Yamazaki, Shin -- Pendergast, Julie S -- Landry, Glenn J -- Takumi, Toru -- Nakamura, Wataru -- NS051278/NS/NINDS NIH HHS/ -- R01 NS051278/NS/NINDS NIH HHS/ -- R01 NS051278-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):675; author reply 675. doi: 10.1126/science.1161284.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada. mistlber@sfu.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974333" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Behavior, Animal ; Biological Clocks/*physiology ; Circadian Rhythm/*physiology ; Cues ; Darkness ; Dorsomedial Hypothalamic Nucleus/*metabolism ; *Food ; *Light ; Mice ; Mutation
    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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    Detection of T cell responses to a ubiquitous cellular protein in autoimmune disease (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-10-18
    Description: T cells that mediate autoimmune diseases such as rheumatoid arthritis (RA) are difficult to characterize because they are likely to be deleted or inactivated in the thymus if the self antigens they recognize are ubiquitously expressed. One way to obtain and analyze these autoimmune T cells is to alter T cell receptor (TCR) signaling in developing T cells to change their sensitivity to thymic negative selection, thereby allowing their thymic production. From mice thus engineered to generate T cells mediating autoimmune arthritis, we isolated arthritogenic TCRs and characterized the self antigens they recognized. One of them was the ubiquitously expressed 60S ribosomal protein L23a (RPL23A), with which T cells and autoantibodies from RA patients reacted. This strategy may improve our understanding of the underlying drivers of autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Yoshinaga -- Hashimoto, Motomu -- Hirota, Keiji -- Ohkura, Naganari -- Morikawa, Hiromasa -- Nishikawa, Hiroyoshi -- Tanaka, Atsushi -- Furu, Moritoshi -- Ito, Hiromu -- Fujii, Takao -- Nomura, Takashi -- Yamazaki, Sayuri -- Morita, Akimichi -- Vignali, Dario A A -- Kappler, John W -- Matsuda, Shuichi -- Mimori, Tsuneyo -- Sakaguchi, Noriko -- Sakaguchi, Shimon -- R01 DK089125/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):363-8. doi: 10.1126/science.1259077.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. ; Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of the Control for Rheumatic Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. ; Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of Frontier Research in Tumor Immunology, Center of Medical Innovation and Translational Research, Osaka University, Osaka 565-0871, Japan. ; Department of the Control for Rheumatic Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. Department of Orthopaedic Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of the Control for Rheumatic Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Geriatric and Environmental Dermatology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. ; Integrated Department of Immunology, National Jewish Health, Denver, CO 80206, USA. Howard Hughes Medical Institute, National Jewish Health, Denver, CO 80206, USA. ; Department of Orthopaedic Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Tokyo 102-0075, Japan. shimon@ifrec.osaka-u.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/genetics/*immunology ; Autoantigens/*immunology ; Autoimmunity/*immunology ; DNA-Binding Proteins/genetics ; Gene Expression Regulation ; Genes, T-Cell Receptor beta ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Receptors, Antigen, T-Cell/*immunology ; Ribosomal Proteins/genetics/*immunology ; T-Lymphocytes/*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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  • 5
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    Hoxb5 marks long-term haematopoietic stem cells and reveals a homogenous perivascular niche (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-02-13
    Description: Haematopoietic stem cells (HSCs) are arguably the most extensively characterized tissue stem cells. Since the identification of HSCs by prospective isolation, complex multi-parameter flow cytometric isolation of phenotypic subsets has facilitated studies on many aspects of HSC biology, including self-renewal, differentiation, ageing, niche, and diversity. Here we demonstrate by unbiased multi-step screening, identification of a single gene, homeobox B5 (Hoxb5, also known as Hox-2.1), with expression in the bone marrow that is limited to long-term (LT)-HSCs in mice. Using a mouse single-colour tri-mCherry reporter driven by endogenous Hoxb5 regulation, we show that only the Hoxb5(+) HSCs exhibit long-term reconstitution capacity after transplantation in primary transplant recipients and, notably, in secondary recipients. Only 7-35% of various previously defined immunophenotypic HSCs are LT-HSCs. Finally, by in situ imaging of mouse bone marrow, we show that 〉94% of LT-HSCs (Hoxb5(+)) are directly attached to VE-cadherin(+) cells, implicating the perivascular space as a near-homogenous location of LT-HSCs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, James Y -- Miyanishi, Masanori -- Wang, Sean K -- Yamazaki, Satoshi -- Sinha, Rahul -- Kao, Kevin S -- Seita, Jun -- Sahoo, Debashis -- Nakauchi, Hiromitsu -- Weissman, Irving L -- F30-HL122096/HL/NHLBI NIH HHS/ -- R01 CA086065/CA/NCI NIH HHS/ -- R01 HL058770/HL/NHLBI NIH HHS/ -- T32 GM007365/GM/NIGMS NIH HHS/ -- U01 HL099999/HL/NHLBI NIH HHS/ -- England -- Nature. 2016 Feb 11;530(7589):223-7. doi: 10.1038/nature16943.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. ; Ludwig Center for Cancer Stem Cell Research and Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. ; Division of Stem Cell Therapy, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863982" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Biomarkers/analysis ; Bone Marrow/metabolism ; Cadherins/metabolism ; Cell Self Renewal ; Gene Expression Regulation ; Genes, Reporter/genetics ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/*metabolism ; Homeodomain Proteins/genetics/*metabolism ; Immunophenotyping ; Male ; Mice ; Mice, Inbred C57BL ; *Stem Cell Niche
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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