CST, 12117S, ITCH (D8Q6D) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying ITCH. Validated for Western Blotting,Immunoprecipitation. Available in 2 sizes. Highly specific and rigorously validated in-house, ITCH (D8Q6D) Rabbit Monoclonal Antibody (CST #12117) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunoprecipitation: 1:200 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting, Immunoprecipitation Specificity / Sensitivity ITCH (D8Q6D) Rabbit Monoclonal Antibody recognizes endogenous levels of total ITCH protein. Species Reactivity: Human, Mouse, Rat Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp125 of human ITCH protein. Background ITCH is a HECT domain-containing E3 ubiquitin ligase, first identified in genetic studies of the mouse locus, in which mutations result in characteristic coat color changes. One particular mutation (non-agouti-lethal 18H) is notable for the development of immunological defects not observed in other mutant mice; these include lymphoid hyperplasia and chronic stomach, lung and skin inflammation (manifest as constant itching). The 18H mutation was traced to a chromosomal inversion that disrupted expression of an adjacent gene in the locus, subsequently termed to reflect the chronic itching phenotype (1-3). Further characterizations revealed that encoded a NEDD4-like E3-ubiquitin ligase capable of catalyzing Lys29, Lys48, and/or Lys63-linked ubiquitination of target proteins, leading to their degradation by the proteosome pathway (4-6). The distinct phenotypes of mutant mice led to the identification of an important regulatory role for ITCH-mediated ubiquitination in inflammatory signaling pathways. For example, ITCH-mediated ubiquitination of the transcription factor JunB was shown to play a direct inhibitory role in regulating expression of the proinflammatory cytokine IL-4. ITCH-null T lymphocytes consequently exhibit increased production of IL-4, leading to biased differentiation of naive CD4 cells towards the proinflammatory Th2 lineage (7). In accordance with the findings from mutant mouse models, a genetic linkage study in humans identified loss-of-function mutations in as a direct cause of syndromic multisystem autoimmune disease (SMAD) (8). Notably, targets of ITCH-mediated ubiquitination are not restricted to immune signaling pathways. For example, key mediators of the Hedgehog (9,10), Wnt/β-catenin (11), Hippo (12), and Notch signaling pathways (13,14) have been identified as important targets of ITCH-mediated ubiquitination (2). Alternate Names ADMFD; AIF4; AIP4; atrophin-1 interacting protein 4; Atrophin-1-interacting protein 4; dJ468O1.1; dJ468O1.1 (atrophin 1 interacting protein 4 (AIP4)); E3 ubiquitin-protein ligase Itchy homolog; HECT-type E3 ubiquitin transferase Itchy homolog; ITCH; itchy E3 ubiquitin protein ligase; itchy E3 ubiquitin protein ligase homolog; itchy E3 ubiquitin protein ligase homolog (mouse); itchy homolog E3 ubiquitin protein ligase; NAPP1; NFE2-associated polypeptide 1; ubiquitin protein ligase ITCH Specification REACTIVITY: H M R SENSITIVITY: Endogenous MW (kDa): 105 Source/Isotype: Rabbit IgG