|Calculated MW||26722 Da|
|Other Names||Complement C1q subcomponent subunit B, C1QB|
|Target/Specificity||A synthetic peptide corresponding to residues in 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.|
|Function||C1q associates with the proenzymes C1r and C1s to yield C1, the first component of the serum complement system. The collagen-like regions of C1q interact with the Ca(2+)-dependent C1r(2)C1s(2) proenzyme complex, and efficient activation of C1 takes place on interaction of the globular heads of C1q with the Fc regions of IgG or IgM antibody present in immune complexes.|
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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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