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  • 1
    Publication Date: 2000-08-11
    Description: Wnts are secreted signaling proteins that regulate developmental processes. Here we show that Wnt signaling, likely mediated by Wnt-10b, is a molecular switch that governs adipogenesis. Wnt signaling maintains preadipocytes in an undifferentiated state through inhibition of the adipogenic transcription factors CCAAT/enhancer binding protein alpha (C/EBPalpha) and peroxisome proliferator- activated receptor gamma (PPARgamma). When Wnt signaling in preadipocytes is prevented by overexpression of Axin or dominant-negative TCF4, these cells differentiate into adipocytes. Disruption of Wnt signaling also causes transdifferentiation of myoblasts into adipocytes in vitro, highlighting the importance of this pathway not only in adipocyte differentiation but also in mesodermal cell fate determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ross, S E -- Hemati, N -- Longo, K A -- Bennett, C N -- Lucas, P C -- Erickson, R L -- MacDougald, O A -- 5P60 DK20572/DK/NIDDK NIH HHS/ -- R01-DK51563/DK/NIDDK NIH HHS/ -- T32-DK07245/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Aug 11;289(5481):950-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-0622, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10937998" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/*cytology/*metabolism ; Animals ; Axin Protein ; CCAAT-Enhancer-Binding Proteins ; Cell Differentiation ; Cell Lineage ; Cytoskeletal Proteins/metabolism ; DNA-Binding Proteins/antagonists & inhibitors/genetics/metabolism ; Gene Transfer Techniques ; Genetic Vectors ; Mesoderm/cytology ; Mice ; Mice, Nude ; Muscles/cytology/metabolism ; Nuclear Proteins/antagonists & inhibitors/genetics/metabolism ; Proteins/genetics/metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/metabolism ; *Repressor Proteins ; Retroviridae/genetics/physiology ; *Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/antagonists & inhibitors/genetics/metabolism ; Wnt Proteins ; *Zebrafish Proteins ; beta Catenin
    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: 1993-04-23
    Description: Surface expression of the CD45 tyrosine phosphatase is essential for the T cell antigen receptor (TCR) to couple optimally with its second messenger pathways. CD45 may be required to dephosphorylate a TCR-activated protein tyrosine kinase, which then transduces an activation signal from the TCR. A chimeric molecule that contained extracellular and transmembrane sequences from an allele of a major histocompatibility class I molecule and cytoplasmic sequences of CD45 restored TCR signaling in a CD45-deficient mutant T cell line. Thus, expression of the complex extracellular domain of CD45 is not required for the TCR to couple to its signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hovis, R R -- Donovan, J A -- Musci, M A -- Motto, D G -- Goldman, F D -- Ross, S E -- Koretzky, G A -- CA56050-01/CA/NCI NIH HHS/ -- CA56843-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):544-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8475387" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD45/genetics/*metabolism ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Enzyme Activation ; Humans ; Inositol Phosphates/metabolism ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; *Signal Transduction ; T-Lymphocytes/*metabolism ; Transfection ; Tyrosine/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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