|Calculated MW||39578 Da|
|Other Names||Tribbles homolog 3, TRB-3, Neuronal cell death-inducible putative kinase, SINK, p65-interacting inhibitor of NF-kappa-B, TRIB3, C20orf97, NIPK, SKIP3, TRB3|
|Target/Specificity||A synthetic peptide corresponding to residues on the C terminus of human TRIB3 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||TRIB3 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.
Tribbles homolog 3 (Drosophila), TRIB3, is a putative protein kinase that has been implicated in the regulation of several biological processes in mammalian cells through its ability to influence Akt and other signaling pathways. It is an important negative regulator of adipogenesis because it acts at an early step in the differentiation cascade to block the C/EBP beta proadipogenic function. TRIB3 disrupts insulin signaling by binding directly to Akt and blocking activation of the kinase, thus contributing to insulin resistance in individuals with susceptibility to type II diabetes. TRIB3 expression is remarkably reduced in prostate cancer PC-3 cells after inhibition of phosphatidylinositol (PI) 3-kinase. The expression of TRIB3 is controlled by nutrient supplies, where the lack of glucose or amino acids results in a substantial increase in TRIB3 protein levels in a PI 3-kinase-dependent manner (1-3).
1. Schwarzer R, et al. Cell Signal. 18(6):899-909, 2006
2. Bezy O, et al. Molecular and Cellular Biology 27(19):6818-6831, 2007
3. Du K, et al. Science 300(5625):1574 - 1577, 2003
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