TBC1D4 Antilichaam

TBC1D4 Antibody: TBC1D4, also known as the Akt substrate AS160, was initially identified as an Akt substrate containing a GTPase-activating domain that regulates GLUT4 trafficking, with activation following insulin stimulation. TBC1D4 truncations in humans is a major cause of dominant inherited insulin resistance. The loss of TBC1D4 results in the accumulation of GLUT4 in compartments that are primed for fusion in basal adipocytes.

9882

O60343

NP_055647

Human

Unconjugated

Primary Antibodies

Homeostasis

TBC1D4 Antibody is affinity chromatography purified via peptide column.

Cat. No. 10-635 - Human Prostate Tissue Slide

1 mg/mL

Predicted species reactivity based on immunogen sequence: Mouse: (89%)

TBC1D4 Antibody is supplied in PBS containing 0.02% sodium azide.

None

Blue Ice

TBC1D4 antibody can be stored at 4˚ C for three months and -20˚ C, stable for up to one year.

IgG

TBC1D4

TBC1 domain family, member 4

Homo sapiens

Kane S, Sano H, Liu SCH, et al. Akt phosphorylates a novel adipocyte protein with a Rab GTPase-activating protein (GAP) domain. J. Biol. Chem. 2002; 277:22115-8.

Sano H, Kane S, Sano E, et al. Insulin-stimulated phosphorylation of a Rab GTPase-activating protein regulates GLUT4 translocation. J. Biol. Chem. 2003; 278:14599-602.

Dash S, Sano H, Rochford JJ, et al. A truncation mutation in TBC1D4 in a family with acanthosis nigricans and postprandial hyperinsulinemia. Proc. Natl. Acad. Sci. U.S.A. 2009; 106:9350–5.

Brewer PD, Romenskaia I, Kanow MA, et al. Loss of AS160 Akt substrate causes Glut4 protein to accumulate in compartments that are primed for fusion in basal adipocytes. J. Biol. Chem. 2011; 286:26287-97.

TBC1D4 Antibody: AS160, AS160, KIAA0603, TBC1 domain family member 4, Akt substrate of 160 kDa

ELISA, IHC-P

114688046

Liquid