The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 1 µg/ml. Predicted molecular weight: 76 kDa.
Adapter linking MAP3K7/TAK1 and TRAF6. Promotes MAP3K7 activation in the IL1 signaling pathway. The binding of 'Lys-63'-linked polyubiquitin chains to TAB2 promotes autophosphorylation of MAP3K7 at 'Thr-187'. Involved in heart development.
Widely expressed. In the embryo, expressed in the ventricular trabeculae, endothelial cells of the conotruncal cushions of the outflow tract and in the endothelial cells lining the developing aortic valves.
Involvement in disease
Defects in TAB2 are the cause of congenital heart disease non-syndromic type 2 (CHTD2) [MIM:612863]. It is a disease characterized by congenital developmental abnormalities involving structures of the heart. Clinical features include left ventricular outflow tract obstruction, subaortic stenosis, residual aortic regurgitation, atrial fibrillation, bicuspid aortic valve and aortic dilation. Note=A chromosomal aberration involving TAB2 has been found in a family with congenital heart disease. Translocation t(2;6)(q21;q25).
Shi Y et al. Overexpression of miR-155-5p Inhibits the Proliferation and Migration of IL-13-Induced Human Bronchial Smooth Muscle Cells by Suppressing TGF-ß-Activated Kinase 1/MAP3K7-Binding Protein 2. Allergy Asthma Immunol Res10:260-267 (2018).
Read more (PubMed: 29676073) »
Lin Y & Luo Z NLRP6 facilitates the interaction between TAB2/3 and TRIM38 in rheumatoid arthritis fibroblast-like synoviocytes. FEBS Lett591:1141-1149 (2017).
Read more (PubMed: 28295271) »