The gene IP6K1 (inositol hexakisphosphate kinase 1), also referred to as IHPK1, is mapped to human chromosome 3p21.31. The 1323bp open reading frame contains six exons that encode a protein of 441 amino acids. It is found to be expressed in several tissues, such as testis, brain, heart, pancreas, liver, kidney, and skeletal muscle.
Immunogen
synthetic peptide corresponding to amino acids 216-233 of human IP6 kinase.
Biochem/physiol Actions
The gene IP6K1 (inositol hexakisphosphate kinase 1) encodes a member of the inositol hexakisphosphate kinases (InsP6K) that also comprise of InsP6K2, and InsP6K3. The members of this family are involved in the conversion of InsP6 (phytic acid) to InsP7 (diphosphoinositol-pentakisphosphate), which functions in vesicular trafficking and exocytosis, apoptosis, and insulin disposition. Knock-out of this gene in mice has been shown to increase insulin sensitivity due to a decrease in the levels of InsP7, a physiologic inhibitor of Akt, a serine/threonine protein kinase that regulates glucose homeostasis. IP6K1 is found to negatively regulate PtdIns(3,4,5)P3 signaling, which in turn, regulates the function of neutrophils in innate immunity.
Physical form
100 μg of affinity isolated IgG in PBS with 1.0 mg/ml bovine serum albumin and 0.05% sodium azide.
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Inositol phosphates are widely produced throughout animal and plant tissues. Diphosphoinositol pentakisphosphate (InsP7) contains an energetic pyrophosphate bond. Here we demonstrate that disruption of inositol hexakisphosphate kinase 1 (InsP6K1), one of the three mammalian inositol hexakisphosphate kinases (InsP6Ks) that convert
Journal of human genetics, 49(7), 360-365 (2004-06-29)
Type 2 diabetes mellitus (T2DM) is a group of multifactorial disorders due to either defective insulin secretion or action. Despite the fact that numerous genetic researches of T2DM have been pursued, the pathogenic mechanisms remain obscure. We encountered a T2DM
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