|Other Names||TGF-beta-activated kinase 1 and MAP3K7-binding protein 1, Mitogen-activated protein kinase kinase kinase 7-interacting protein 1, TGF-beta-activated kinase 1-binding protein 1, TAK1-binding protein 1, TAB1, MAP3K7IP1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP6861c was selected from the region of human MAP3K7IP1-pS438. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||May be an important signaling intermediate between TGFB receptors and MAP3K7/TAK1. May play an important role in mammalian embryogenesis.|
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Provided below are standard protocols that you may find useful for product applications.
MAP3K7IP1 was identified as a regulator of the MAP kinase kinase kinase MAP3K7/TAK1, which is known to mediate various intracellular signaling pathways, such as those induced by TGF beta, interleukin 1, and WNT-1. This protein interacts and thus activates TAK1 kinase. It has been shown that the C-terminal portion of this protein is sufficient for binding and activation of TAK1, while a portion of the N-terminus acts as a dominant-negative inhibitor of TGF beta, suggesting that this protein may function as a mediator between TGF beta receptors and TAK1. This protein can also interact with and activate the mitogen-activated protein kinase 14 (MAPK14/p38alpha), and thus represents an alternative activation pathway, in addition to the MAPKK pathways, which contributes to the biological responses of MAPK14 to various stimuli.
Arch,R.H., et.al., Genes Dev. 12 (18), 2821-2830 (1998)Yamaguchi,K., et.al., EMBO J. 18 (1), 179-187 (1999)
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