|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_066981, 31542265|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||Predicted: 39 kDa |
Observed: 39 kDa
|Application Notes||TRB3 antibody can be used for detection of TRB3 by Western blot at 1 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Target/Specificity||TRB3; TRB3 antibody is human, mouse and rat reactive. At least two isoforms of TRB3 are known to exist; this antibody will detect both isoforms.|
|Reconstitution & Storage||TRB3 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year.|
|Precautions||TRB3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||C20orf97, NIPK, SKIP3, TRB3|
|Function||Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1. Binds to ATF4 and inhibits its transcriptional activation activity. Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. Interacts with MAPK kinases and regulates activation of MAP kinases. May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. Does not display kinase activity. Inhibits the transcriptional activity of DDIT3/CHOP and is involved in DDIT3/CHOP-dependent cell death during ER stress. Can inhibit APOBEC3A editing of nuclear DNA.|
|Tissue Location||Highest expression in liver, pancreas, peripheral blood leukocytes and bone marrow. Also highly expressed in a number of primary lung, colon and breast tumors. Expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney.|
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Provided below are standard protocols that you may find useful for product applications.
TRB3 was initially identified as a novel kinase-like gene that was overexpressed in multiple human tumors and regulated by hypoxia (1). In the liver, TRB3 binds and inhibits AKT activity, leading to impaired insulin signaling (2), whereas in adipose tissue TRB3 is involved in the regulation of fatty acid oxidation through ubiquitination of Acetyl-CoA carboxylase (3). Endoplasmic reticulum (ER) stress induces TRB3 expression in skeletal muscle, leading to a decrease in insulin signaling and glucose uptake, suggesting that inhibition of TRB3 expression may be a potential therapeutic treatment for managing insulin resistance (4).
Bowers AJ, Scully S, and Boylan JF. SKIP3, a novel drosophila tribbles ortholog, is overexpressed in human tumors and is regulated by hypoxia. Oncogene 2003; 22:2823-35.
Du K, Herzig S, Kulkarni RN, et al. TRB3: a tribbles homolog that inhibits Akt/PKB activation by insulin in liver. Science 2003; 300:1574-7.
Qi L, Heredia JE, Altarejos JY, et al. TRB3 inks the E3 ubiquitin ligase COP1 to lipid metabolism. Science 2006; 312:1763-6.
Koh HJ, Toyoda T, Didesch MM, et al. Tribbles 3 mediates endoplasmic reticulum stress-induced insulin resistance in skeletal muscle. Nat. Commun. 2013; 4:1871.
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