Targeted inactivation of GPR26 leads to hyperphagia and adiposity by activating AMPK in the hypothalamus.
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Genetic variants associated with motion sickness point to roles for inner ear development, neurological processes and glucose homeostasis.Hunting for the function of orphan GPCRs - beyond the search for the endogenous ligand.Neuro-psychopharmacological perspective of Orphan receptors of Rhodopsin (class A) family of G protein-coupled receptors.Neanderthal-Derived Genetic Variation Shapes Modern Human Cranium and Brain.Evidence of alterations in the expression of orphan receptors GPR26 and GPR39 due to the etiology of the metabolic syndrome.
P2860
Targeted inactivation of GPR26 leads to hyperphagia and adiposity by activating AMPK in the hypothalamus.
description
2012 nî lūn-bûn
@nan
2012 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@ast
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@en
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@nl
type
label
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@ast
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@en
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@nl
prefLabel
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@ast
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@en
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@nl
P2093
P2860
P1433
P1476
Targeted inactivation of GPR26 ...... ting AMPK in the hypothalamus.
@en
P2093
Daohong Chen
Weiping Zhang
Xiaolei Liu
Yuguang Shi
P2860
P304
P356
10.1371/JOURNAL.PONE.0040764
P407
P577
2012-07-16T00:00:00Z