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  • 1
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    CRTC3 links catecholamine signalling to energy balance (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-12-18
    Beschreibung: The adipose-derived hormone leptin maintains energy balance in part through central nervous system-mediated increases in sympathetic outflow that enhance fat burning. Triggering of beta-adrenergic receptors in adipocytes stimulates energy expenditure by cyclic AMP (cAMP)-dependent increases in lipolysis and fatty-acid oxidation. Although the mechanism is unclear, catecholamine signalling is thought to be disrupted in obesity, leading to the development of insulin resistance. Here we show that the cAMP response element binding (CREB) coactivator Crtc3 promotes obesity by attenuating beta-adrenergic receptor signalling in adipose tissue. Crtc3 was activated in response to catecholamine signals, when it reduced adenyl cyclase activity by upregulating the expression of Rgs2, a GTPase-activating protein that also inhibits adenyl cyclase activity. As a common human CRTC3 variant with increased transcriptional activity is associated with adiposity in two distinct Mexican-American cohorts, these results suggest that adipocyte CRTC3 may play a role in the development of obesity in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025711/" 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/PMC3025711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Youngsup -- Altarejos, Judith -- Goodarzi, Mark O -- Inoue, Hiroshi -- Guo, Xiuqing -- Berdeaux, Rebecca -- Kim, Jeong-Ho -- Goode, Jason -- Igata, Motoyuki -- Paz, Jose C -- Hogan, Meghan F -- Singh, Pankaj K -- Goebel, Naomi -- Vera, Lili -- Miller, Nina -- Cui, Jinrui -- Jones, Michelle R -- CHARGE Consortium -- GIANT Consortium -- Chen, Yii-Der I -- Taylor, Kent D -- Hsueh, Willa A -- Rotter, Jerome I -- Montminy, Marc -- M01 RR000425-36/RR/NCRR NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- N01 HC095159/HC/NHLBI NIH HHS/ -- N01-HC95159/HC/NHLBI NIH HHS/ -- N02 HL64278/HL/NHLBI NIH HHS/ -- N02-HL64278/HL/NHLBI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-09/DK/NIDDK NIH HHS/ -- P30-DK063491/DK/NIDDK NIH HHS/ -- R01 DK033651/DK/NIDDK NIH HHS/ -- R01 DK049777/DK/NIDDK NIH HHS/ -- R01 DK049777-18/DK/NIDDK NIH HHS/ -- R01 DK079888/DK/NIDDK NIH HHS/ -- R01 DK079888-05/DK/NIDDK NIH HHS/ -- R01 HL071205/HL/NHLBI NIH HHS/ -- R01 HL071205-05/HL/NHLBI NIH HHS/ -- R01 HL088457/HL/NHLBI NIH HHS/ -- R01 HL088457-04/HL/NHLBI NIH HHS/ -- R01-DK049777/DK/NIDDK NIH HHS/ -- R01-DK083834/DK/NIDDK NIH HHS/ -- R01-DK79888/DK/NIDDK NIH HHS/ -- R01-HL088457/HL/NHLBI NIH HHS/ -- R01-L071205/PHS HHS/ -- R37 DK083834/DK/NIDDK NIH HHS/ -- R37 DK083834-26/DK/NIDDK NIH HHS/ -- R37 DK083834-27/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Dec 16;468(7326):933-9. doi: 10.1038/nature09564.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164481" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipocytes/drug effects/metabolism ; Adipose Tissue/drug effects/metabolism ; Animals ; Body Temperature ; Catecholamines/*metabolism ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/antagonists & inhibitors/metabolism ; Dietary Fats/pharmacology ; *Energy Metabolism/genetics ; Female ; Genome-Wide Association Study ; Humans ; Insulin Resistance ; Mexican Americans/genetics ; Mice ; Obesity/chemically induced/genetics/metabolism ; Phosphorylation ; RGS Proteins/biosynthesis/genetics ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/drug effects/*physiology ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Coronin 2A mediates actin-dependent de-repression of inflammatory response genes (2011)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2011-02-19
    Beschreibung: Toll-like receptors (TLRs) function as initiators of inflammation through their ability to sense pathogen-associated molecular patterns and products of tissue damage. Transcriptional activation of many TLR-responsive genes requires an initial de-repression step in which nuclear receptor co-repressor (NCoR) complexes are actively removed from the promoters of target genes to relieve basal repression. Ligand-dependent SUMOylation of liver X receptors (LXRs) has been found to suppress TLR4-induced transcription potently by preventing the NCoR clearance step, but the underlying mechanisms remain enigmatic. Here we provide evidence that coronin 2A (CORO2A), a component of the NCoR complex of previously unknown function, mediates TLR-induced NCoR turnover by a mechanism involving interaction with oligomeric nuclear actin. SUMOylated LXRs block NCoR turnover by binding to a conserved SUMO2/SUMO3-interaction motif in CORO2A and preventing actin recruitment. Intriguingly, the LXR transrepression pathway can itself be inactivated by inflammatory signals that induce calcium/calmodulin-dependent protein kinase IIgamma (CaMKIIgamma)-dependent phosphorylation of LXRs, leading to their deSUMOylation by the SUMO protease SENP3 and release from CORO2A. These findings uncover a CORO2A-actin-dependent mechanism for the de-repression of inflammatory response genes that can be differentially regulated by phosphorylation and by nuclear receptor signalling pathways that control immunity and homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3464905/" 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/PMC3464905/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Ghisletti, Serena -- Saijo, Kaoru -- Gandhi, Meghal -- Aouadi, Myriam -- Tesz, Greg J -- Zhang, Dawn X -- Yao, Joyee -- Czech, Michael P -- Goode, Bruce L -- Rosenfeld, Michael G -- Glass, Christopher K -- 1F31DK083913/DK/NIDDK NIH HHS/ -- CA52599/CA/NCI NIH HHS/ -- DK074868/DK/NIDDK NIH HHS/ -- DK085853/DK/NIDDK NIH HHS/ -- HC088093/HC/NHLBI NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P50 HL056989/HL/NHLBI NIH HHS/ -- R01 CA052599/CA/NCI NIH HHS/ -- R01 CA097134/CA/NCI NIH HHS/ -- R01 DK091183/DK/NIDDK NIH HHS/ -- R01 HL065445/HL/NHLBI NIH HHS/ -- R01 NS034934/NS/NINDS NIH HHS/ -- R37 DK039949/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 17;470(7334):414-8. doi: 10.1038/nature09703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21331046" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/chemistry/*metabolism ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cell Line ; *Gene Expression Regulation/drug effects ; Gene Knockdown Techniques ; HeLa Cells ; Homeostasis/genetics ; Humans ; Inflammation/*genetics ; Lipopolysaccharides/pharmacology ; Mice ; Microfilament Proteins/chemistry/deficiency/genetics/*metabolism ; Orphan Nuclear Receptors/metabolism ; Peptide Hydrolases/metabolism ; Peritonitis/chemically induced/metabolism ; Phosphorylation ; Promoter Regions, Genetic/genetics ; Protein Structure, Tertiary ; Signal Transduction ; Sumoylation ; Thioglycolates/pharmacology ; Toll-Like Receptors/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Inositol-1,4,5-trisphosphate receptor regulates hepatic gluconeogenesis in fasting and diabetes (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-04-13
    Beschreibung: In the fasted state, increases in circulating glucagon promote hepatic glucose production through induction of the gluconeogenic program. Triggering of the cyclic AMP pathway increases gluconeogenic gene expression via the de-phosphorylation of the CREB co-activator CRTC2 (ref. 1). Glucagon promotes CRTC2 dephosphorylation in part through the protein kinase A (PKA)-mediated inhibition of the CRTC2 kinase SIK2. A number of Ser/Thr phosphatases seem to be capable of dephosphorylating CRTC2 (refs 2, 3), but the mechanisms by which hormonal cues regulate these enzymes remain unclear. Here we show in mice that glucagon stimulates CRTC2 dephosphorylation in hepatocytes by mobilizing intracellular calcium stores and activating the calcium/calmodulin-dependent Ser/Thr-phosphatase calcineurin (also known as PP3CA). Glucagon increased cytosolic calcium concentration through the PKA-mediated phosphorylation of inositol-1,4,5-trisphosphate receptors (InsP(3)Rs), which associate with CRTC2. After their activation, InsP(3)Rs enhanced gluconeogenic gene expression by promoting the calcineurin-mediated dephosphorylation of CRTC2. During feeding, increases in insulin signalling reduced CRTC2 activity via the AKT-mediated inactivation of InsP(3)Rs. InsP(3)R activity was increased in diabetes, leading to upregulation of the gluconeogenic program. As hepatic downregulation of InsP(3)Rs and calcineurin improved circulating glucose levels in insulin resistance, these results demonstrate how interactions between cAMP and calcium pathways at the level of the InsP(3)R modulate hepatic glucose production under fasting conditions and in diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3343222/" 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/PMC3343222/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yiguo -- Li, Gang -- Goode, Jason -- Paz, Jose C -- Ouyang, Kunfu -- Screaton, Robert -- Fischer, Wolfgang H -- Chen, Ju -- Tabas, Ira -- Montminy, Marc -- HL087123/HL/NHLBI NIH HHS/ -- P01 HL087123/HL/NHLBI NIH HHS/ -- P01 HL087123-05/HL/NHLBI NIH HHS/ -- R01 DK049777/DK/NIDDK NIH HHS/ -- R01 DK049777-19/DK/NIDDK NIH HHS/ -- R01 DK091618/DK/NIDDK NIH HHS/ -- R01 DK091618-02/DK/NIDDK NIH HHS/ -- R01-DK049777/DK/NIDDK NIH HHS/ -- R01-DK083834/DK/NIDDK NIH HHS/ -- R01-DK091618/DK/NIDDK NIH HHS/ -- R37 DK083834/DK/NIDDK NIH HHS/ -- R37 DK083834-29/DK/NIDDK NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Apr 8;485(7396):128-32. doi: 10.1038/nature10988.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495310" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blood Glucose/*metabolism ; Calcineurin/metabolism ; Calcium/metabolism ; Calcium Signaling ; Cells, Cultured ; Cyclic AMP/metabolism ; Diabetes Mellitus/blood/genetics/*metabolism ; Fasting/blood/*metabolism ; Gene Expression Regulation/drug effects ; Glucagon/pharmacology ; *Gluconeogenesis/genetics ; HEK293 Cells ; Hepatocytes/metabolism ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/*metabolism ; Insulin Resistance ; Liver/cytology/*metabolism ; Mice ; Phosphorylation/drug effects ; Trans-Activators/metabolism ; Transcription Factors
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
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