ITCH Protéine
Aperçu rapide pour ITCH Protéine (ABIN7317650)
Antigène
Voir toutes ITCH ProtéinesType de proteíne
Origine
Source
Pureté
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Fonction
- Recombinant Human ITCH/AIP4 Protein (aa 526-903)
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Séquence
- Arg 526-Glu 903
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Attributs du produit
- A DNA sequence encoding the human ITCH (NP_113671.3) N-terminal segment (Arg 526-Glu 903) was expressed and purified, with two additional amino acids (Gly & Pro) at the N-terminus.
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Restrictions
- For Research Use only
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Format
- Lyophilized
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Reconstitution
- Please refer to the printed manual for detailed information.
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Buffer
- Lyophilized from sterile 20 mM Tris, 200 mM NaCl, 10 % glycerol, pH 8.0
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Stock
- 4 °C,-20 °C,-80 °C
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Stockage commentaire
- Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80°C. Reconstituted protein solution can be stored at 4-8°C for 2-7 days. Aliquots of reconstituted samples are stable at < -20°C for 3 months.
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- ITCH (Itchy E3 Ubiquitin Protein Ligase Homolog (ITCH))
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Autre désignation
- ITCH/AIP4
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Sujet
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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.
Synonym: ADMFD;AIF4;AIP4;dJ468O1.1;NAPP1
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Poids moléculaire
- 40 kDa
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NCBI Accession
- NP_113671
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Pathways
- Activation of Innate immune Response, CXCR4-mediated Signaling Events
Antigène
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