ITCH / AIP4抗体

ITCH / AIP4抗体产品信息

免疫原 :
Recombinant Human ITCH / AIP4 protein (Catalog#11131-HNCE)
Reagents : PE-conjugated mouse monoclonal antibody
Clone ID :
01
抗体宿主 :
Mouse IgG1
Concentration :
5 μl/Test, 0.1 mg/ml
缓冲液 : Aqueous solution containing 0.5% BSA and 0.09% sodium azide
制备方法 :
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human ITCH / AIP4 (rh ITCH / AIP4; Catalog#11131-HNCE; NP_113671.3; Arg 526-Glu 903) and conjugated with PE under optimum conditions, the unreacted PE was removed.
ITCH / AIP4抗体Background
E3 ubiquitin-protein ligase Itchy homolog, also known as Atrophin-1-interacting protein 4, NFE2-associated polypeptide 1, NAPP1 and ITCH, is a cell membrane protein which contains oneC2 domain, oneHECT (E6AP-type E3 ubiquitin-protein ligase) domain and contains fourWW domains. ITCH acts as an E3 ubiquitin-protein ligase which accepts ubiquitin from an E2 ubiquitin-conjugating enzyme in the form of a thioester and then directly transfers the ubiquitin to targeted substrates. It catalyzes 'Lys-29'-, 'Lys-48'- and 'Lys-63'-linked ubiquitin conjugation. ITCH is involved in the control of inflammatory signaling pathways. It is an essential component of a ubiquitin-editing protein complex, comprising also TNFAIP3, TAX1BP1 and RNF11, that ensures the transient nature of inflammatory signaling pathways. ITCH promotes the association of the complex after TNF stimulation. Once the complex is formed, TNFAIP3 deubiquitinates 'Lys-63' polyubiquitin chains on RIPK1 and catalyzes the formation of 'Lys-48'-polyubiquitin chains. This leads to RIPK1 proteosomal degradation and consequently termination of the TNF- or LPS-mediated activation of NFKB1. Defects in ITCH are the cause of syndromic multisystem autoimmune disease (SMAD) which is characterized by organomegaly, failure to thrive, developmental delay, dysmorphic features and autoimmune inflammatory cell infiltration of the lungs, liver and gut.
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