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ITCH / AIP4 Antibody (FITC), Mouse MAb

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ITCHAntibody Product Information
Antigen:Recombinant Human ITCH / AIP4 protein (Catalog#11131-HNCE)
Clone ID:01
Ig Type:Mouse IgG1
Concentration:10 μl/Test, 0.1 mg/ml
Formulation:Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Preparation: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 FITC under optimum conditions, the unreacted FITC was removed.
ITCHAntibody Usage Guide
Specificity:Human ITCH / AIP4
Application:FCM
Storage:This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Images

Flow cytometric analysis of Human ITCH expression in HeLa cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and then stained with FITC Mouse anti-ITCH (11131-MM01-F). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.

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 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.

References
  • Marchese A. et al., 2003, Dev. Cell 5:709-22.
  • Wang Y. et al., 2006, EMBO J. 25: 5058-70.
  • Bhandari D. et al., 2009, Mol. Biol. Cell 20:1324-39.
  • Edwards TL. et al., 2009, Biochem. J. 423:31-9.
  • Zhang P. et al., 2010, J. Biol. Chem. 285:8869-79.
  • Azakir B.A. et al., 2010, FEBS J. 277:1319-30.
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