Overview:
QIK is a serine/threonine protein kinase that contains an N-terminal kinase domain, a central domain with ubiquitin-associate motif, and a C-terminal PKAphosphorylation site. QIK can phosphorylate IRS1 and overexpression of QIK in adipocyte elevates the phosphorylation of IRS1 (1). The QIK-mediated phosphorylation of IRS1 may modulate the efficiency of insulin signal transduction and could be responsible for insulin resistance associated with diabetes (1). Insulin disrupts TORC2 activity by induction of QIK which then stimulates the phosphorylation and cytoplasmic translocation of TORC2. Phosphorylated TORC2 is subsequently degraded by the 26S proteasome (2).
Gene Aliases:
SNF1LK2, SIK2, KIAA0781, LOH11CR1I, DKFZp434K1115
Genbank Number:
NM_015191
References:
1. Horike N, et al: Adipose-specific expression, phosphorylation of ser794 in insulin receptor substrate-1, and activation in diabetic animals of salt-inducible kinase-2. J. Biol. Chem. 278: 18440-18447, 2003. 2. Dentin R, et al: Insulin modulates gluconeogenesis by inhibition of the coactivator TORC2. Nature 449: 366-369, 2007.
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那糖酵解中依赖NAD的酶不是要在线粒体内反应?
蛋白酶分布广泛,主要存在于人和动物消化道中,而消化道通过口与肛门与外界相通,属于外环境或外界环境
(溶菌酶、凝血酶原等)分布在内环境
(消化)酶分布在消化道

