排序方式: 共有27条查询结果,搜索用时 328 毫秒
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Towards a molecular understanding of adaptive thermogenesis 总被引:50,自引:0,他引:50
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PRDM16 controls a brown fat/skeletal muscle switch 总被引:4,自引:0,他引:4
Seale P Bjork B Yang W Kajimura S Chin S Kuang S Scimè A Devarakonda S Conroe HM Erdjument-Bromage H Tempst P Rudnicki MA Beier DR Spiegelman BM 《Nature》2008,454(7207):961-967
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TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis 总被引:2,自引:0,他引:2
Kabashi E Valdmanis PN Dion P Spiegelman D McConkey BJ Vande Velde C Bouchard JP Lacomblez L Pochigaeva K Salachas F Pradat PF Camu W Meininger V Dupre N Rouleau GA 《Nature genetics》2008,40(5):572-574
Recently, TDP-43 was identified as a key component of ubiquitinated aggregates in amyotrophic lateral sclerosis (ALS), an adult-onset neurological disorder that leads to the degeneration of motor neurons. Here we report eight missense mutations in nine individuals--six from individuals with sporadic ALS (SALS) and three from those with familial ALS (FALS)--and a concurring increase of a smaller TDP-43 product. These findings further corroborate that TDP-43 is involved in ALS pathogenesis. 相似文献
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CREB regulates hepatic gluconeogenesis through the coactivator PGC-1 总被引:49,自引:0,他引:49
Herzig S Long F Jhala US Hedrick S Quinn R Bauer A Rudolph D Schutz G Yoon C Puigserver P Spiegelman B Montminy M 《Nature》2001,413(6852):179-183
When mammals fast, glucose homeostasis is achieved by triggering expression of gluconeogenic genes in response to glucagon and glucocorticoids. The pathways act synergistically to induce gluconeogenesis (glucose synthesis), although the underlying mechanism has not been determined. Here we show that mice carrying a targeted disruption of the cyclic AMP (cAMP) response element binding (CREB) protein gene, or overexpressing a dominant-negative CREB inhibitor, exhibit fasting hypoglycaemia [corrected] and reduced expression of gluconeogenic enzymes. CREB was found to induce expression of the gluconeogenic programme through the nuclear receptor coactivator PGC-1, which is shown here to be a direct target for CREB regulation in vivo. Overexpression of PGC-1 in CREB-deficient mice restored glucose homeostasis and rescued expression of gluconeogenic genes. In transient assays, PGC-1 potentiated glucocorticoid induction of the gene for phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme in gluconeogenesis. PGC-1 promotes cooperativity between cyclic AMP and glucocorticoid signalling pathways during hepatic gluconeogenesis. Fasting hyperglycaemia is strongly correlated with type II diabetes, so our results suggest that the activation of PGC-1 by CREB in liver contributes importantly to the pathogenesis of this disease. 相似文献
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