| 货号 | 12117S |
| 反应种属 | Human/Mouse/Rat |
| 来源宿主 | Rabbit |
| 应用 | W/IP |
| 目标/特异性 | ITCH (D8Q6D) Rabbit mAb recognizes endogenous levels of total ITCH protein. |
| 使用方法 | WB(1:1000) IP (1:200) |
| 供应商 | CST |
| 背景 | ITCH is a HECT domain-containing E3 ubiquitin ligase, first identified in genetic studies of the mouse agouti locus, in which mutations result in characteristic coat color changes. One particular agouti mutation (non-agouti-lethal 18H) is notable for the development of immunological defects not observed in other agouti mutant mice; these include lymphoid hyperplasia and chronic stomach, lung and skin inflammation (manifest as constant itching). The 18H agouti mutation was traced to a chromosomal inversion that disrupted expression of an adjacent gene in the agouti locus, subsequently termed Itch to reflect the chronic itching phenotype (1-3). Further characterizations revealed that Itch 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 Itch 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 Itch mouse models, a genetic linkage study in humans identified loss-of-function mutations in ITCH 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). |
| 存放说明 | -20C |
| 计算分子量 | 105 |
Western blot analysis of extracts from various cell lines using ITCH (D8Q6D) Rabbit mAb. Western blot检测多种细胞提取物。 | |
Immunoprecipitation of ITCH from MOLT-4 cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or ITCH (D8Q6D) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using ITCH (D8Q6D) Rabbit mAb. Western blot采用Rabbit (DA1E) mAb IgG XP® 同型对照#3900 (lane 2) 或 ITCH (D8Q6D) Rabbit mAb (lane 3)检测MOLT-4细胞提取物中ITCH。Lane 1中样品浓度为10%。 |
