antibody against itch (Proteintech)
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Antibody Against Itch, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+itch/ITCH+Antibody/10__1096_slash_fj__202502366r-60-19-22
Average 93 stars, based on 28 article reviews
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other:Article Title: E3 ubiquitin ligase ITCH-mediated proteasomal degradation of WBP2 sensitizes breast cancer cells to chemotherapy through restraining AMOTL2/c-JUN axis. Article Snippet: Our study had demonstrated that WW domain-binding protein 2 (WBP2) conferred chemoresistance in breast cancer (BC).. However, the underlying mechanism remains unclear.. Herein, a decreased expression of itchy E3 ubiquitin protein ligase (ITCH) was observed in drug-resistant BC tissues which negatively regulated the expression of WBP2. Article Title: Identification and validation of CDC20 and ITCH as ubiquitination related biomarker in idiopathic pulmonary fibrosis Article Snippet: The antibodies used included Article Title: Identification and validation of CDC20 and ITCH as ubiquitination related biomarker in idiopathic pulmonary fibrosis. Article Snippet: The antibodies used included Article Title: JAC1 suppresses proliferation of breast cancer through the JWA/p38/SMURF1/HER2 signaling Article Snippet: The following antibodies were used: Anti-β-actin, anti-α-tubulin, anti-GAPDH, anti-HA (1;1000, Beyotime, Jiangsu, China); anti-HER2, anti-HER3, anti-p-p38(Thr180/Thr182); anti-Ub (1:1000, CST, USA); anti-JWA (1:100, Laboratory-made); anti-GATA-1, anti-NEDD4, anti-CBL, anti-SMURF1, anti-ITCH, anti-HER1, and Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis Article Snippet: The antibodies used were as follows: Ubiquitin Proteomics:Article Title: Hyper-SUMOylation of SMN induced by SENP2 deficiency decreases its stability and leads to spinal muscular atrophy-like pathology. Article Snippet: Spinal muscular atrophy (SMA), a degenerative motor neuron disease and a leading cause of infant mortality, is caused by loss of functional survival motor neuron (SMN) protein due to SMN1 gene mutation.. Here, using mouse and cell models for behavioral and histological studies, we found that SENP2 (SUMO/sentrin-specific protease 2)-deficient mice developed a notable SMA-like pathology phenotype with significantly decreased muscle fibers and motor neurons.. At the molecular level, SENP2 deficiency in mice did not affect transcription but decreased SMN protein levels by promoting the SUMOylation of SMN. |
