Anti-TBC1 domain family member 4 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.

TBC1D4 antibody was raised against an 19 amino acid peptide near the carboxy terminus of human TBC1D4 . The immunogen is located within amino acids 1190 - 1240 of TBC1D4.

Widely expressed. Isoform 2 is the highest overexpressed in most tissues. Isoform 1 is highly expressed in skeletal muscle and heart, but was not detectable in the liver nor in adipose tissue. Isoform 2 is strongly expressed in adrenal and thyroid gland, and also in lung, kidney, colon, brain and adipose tissue. Isoform 2 is moderately expressed in skeletal muscle. Expressed in pancreatic Langerhans islets, including beta cells (at protein level) . Expression is decreased by twofold in pancreatic islets in type 2 diabetes patients compared to control subjects. Up-regulated in T-cells from patients with atopic dermatitis.

May act as a GTPase-activating protein for RAB2A, RAB8A, RAB10 and RAB14. Isoform 2 promotes insulin-induced glucose transporter SLC2A4/GLUT4 translocation at the plasma membrane, thus increasing glucose uptake.