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ITCH / AIP4 Antibody, Rabbit PAb

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ITCHAntibody Product Information
Immunogen:Recombinant Human ITCH / AIP4 protein (Catalog#11131-HNCE)
Clone ID:
Ig Type:Rabbit IgG
Formulation:0.2 μm filtered solution in PBS with 5% trehalose
Preparation:Produced in rabbits immunized with purified, recombinant Human ITCH / AIP4 (rh ITCH / AIP4; Catalog#11131-HNCE; NP_113671.3; Arg 526-Glu 903). Total IgG was purified by Protein A affinity chromatography.
ITCHAntibody Usage Guide
Specificity:Human ITCH / AIP4

ELISA: 0.5-1 μg/mL

This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human ITCH (526-903). The detection limit for Human ITCH (526-903) is approximately ng/well.

Storage:This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

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 one C2 domain, one HECT (E6AP-type E3 ubiquitin-protein ligase) domain and contains four WW 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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