2dae
From Proteopedia
Solution Structure of the N-terminal CUE Domain in the Human Mitogen-activated Protein Kinase Kinase Kinase 7 Interacting Protein 2 (MAP3K7IP2)
Structural highlights
DiseaseTAB2_HUMAN 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).[1] FunctionTAB2_HUMAN 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.[2] [3] [4] Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. References
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Categories: Homo sapiens | Large Structures | Inoue M | Kigawa T | Koshiba S | Sato M | Yokoyama S | Zhao C
