|Reactivity||Human, Mouse, Rat|
|Calculated MW||146563 Da|
|Positive Control||Jurkat, Rat kidney, 3T3 cell lysates|
|Application & Usage||The antibody can be used for Western blotting (1–4 µg/ml).|
|Other Names||TBC1D4; AS160; DKFZp779C0666|
|Formulation||100 µg (0.5 mg/ml) affinity purified rabbit anti-AS160/TBC1 polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 30% glycerol, 0.5% BSA, 5 mM EDTA and 0.01% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||AS160/TBC1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Cytoplasm. Note=Isoform 2 shows a cytoplasmic perinuclear localization in a myoblastic cell line in resting and insulin-stimulated cells|
|Tissue Location||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.|
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Provided below are standard protocols that you may find useful for product applications.
AS160 is a 160 kDa Akt serine/threonine kinase substrate that plays a critical role in regulating insulin-stimulated exocytosis of glucose transporter GLUT4. Increased in insulin treatment stimulate phophorylation of AS160 that regulates GLUT4 translocation via inactivation of the Rab GTPase function.
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