4.5 Article

Activator of G protein signaling 3 null mice: I. Unexpected alterations in metabolic and cardiovascular function

期刊

ENDOCRINOLOGY
卷 149, 期 8, 页码 3842-3849

出版社

ENDOCRINE SOC
DOI: 10.1210/en.2008-0050

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资金

  1. NCRR NIH HHS [P20-RR021945, P20 RR021945, P20-RR018766, P20 RR018766] Funding Source: Medline
  2. NIDDK NIH HHS [R01 DK074772, DK074772, P30 DK072476] Funding Source: Medline
  3. NIGMS NIH HHS [P30 GM118430] Funding Source: Medline
  4. NIMH NIH HHS [F32MH65092, MH90531, F32 MH065092] Funding Source: Medline
  5. NINDS NIH HHS [NS24821, R01 NS024821] Funding Source: Medline

向作者/读者索取更多资源

Activator of G protein signaling (AGS)-3 plays functional roles in cell division, synaptic plasticity, addictive behavior, and neuronal development. As part of a broad effort to define the extent of functional diversity of AGS3-regulated-events in vivo, we generated AGS3 null mice. Surprisingly, AGS3 null adult mice exhibited unexpected alterations in cardiovascular and metabolic functions without any obvious changes in motor skills, basic behavioral traits, and brain morphology. AGS3 null mice exhibited a lean phenotype, reduced fat mass, and increased nocturnal energy expenditure. AGS3 null mice also exhibited altered blood pressure control mechanisms. These studies expand the functional repertoire for AGS3 and other G protein regulatory proteins providing unexpected mechanisms by which G protein systems may be targeted to influence obesity and cardiovascular function.

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