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中文摘要
翻译
这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者(PI)可能从另一个NIH来源获得主要资金, 因此可以在其他CRISP条目中表示。列出的机构是 中心,不一定是研究者的机构。 细胞内第二信使cAMP作为饥饿状态信号起作用,其介导响应于激素刺激的分解代谢程序的诱导。 禁食的哺乳动物中的葡萄糖平衡例如通过cAMP响应性CREB共活化剂T0 RC 2响应于循环胰高血糖素的升高而诱导促血糖基因来维持。 在进食条件下,TORC 2被隔离在细胞质中,响应于cAMP信号传导,TORC 2被去磷酸化并转移到细胞核,随后它通过相关启动子与CREB结合来刺激基因表达。为了进一步剖析TORC家族在能量平衡中的作用,我们将使用蛋白质组学和遗传学工具来操纵果蝇中的TORC活性。 果蝇TORC相关蛋白的鉴定将为这种共激活因子响应环境信号的机制提供新的见解。
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The intracellular second messenger cAMP functions as a starvation state signal, which mediates induction of catabolic programs in response to hormonal stimulation. Glucose balance in fasted mammals is maintained, for example, by induction of gluconeogenic genes by the cAMP responsive CREB coactivator TORC2 in response to elevations in circulating pancreatic glucagon. Sequestered in the cytoplasm under feeding conditions, TORC2 is dephosphorylated and translocated to the nucleus in response to cAMP signaling, whereupon it stimulates gene expression by associating with CREB over relevant promoters. To further dissect the role of the TORC family in energy balance, we will use proteomic and genetic tools to manipulate TORC activity in Drosophila. The identification of Drosophila TORC-associated proteins will provide new insights into the mechanisms by which this coactivator responds to environmental cues.
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Regulation of Hepatic Gluconeogenesis by the CREB:TORC2 Pathway
Regulation of Hepatic Gluconeogenesis by the CREB:TORC2 Pathway
Regulation of Hepatic Gluconeogenesis by the CREB:TORC2 Pathway
Regulation of Hepatic Gluconeogenesis by the CREB:TORC2 Pathway
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