Ask about this productRelated genes to: ZNF585B Blocking Peptide
- Gene:
- ZNF585B NIH gene
- Name:
- zinc finger protein 585B
- Previous symbol:
- -
- Synonyms:
- FLJ14928, SZFP41
- Chromosome:
- 19q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-15
- Date modifiied:
- 2014-11-19
Related products to: ZNF585B Blocking Peptide
Related articles to: ZNF585B Blocking Peptide
- The carcinogenesis and progression of colon adenocarcinoma (COAD) are intensively related to the abnormal expression of the zinc finger (ZNF) protein genes. We aimed to employ these genes to provide a reliable prognosis and treatment stratification tool for COAD patients. - Source: PubMed
Publication date: 2024/04/25
Xu FanSun JiahuiGu XinyueZhou Qingxin - Enzalutamide, docetaxel, and cabazitaxel treatment resistance is a major problem in metastatic castration resistant prostate cancer (mCRPC), but the underlying genetic determinants are poorly understood. To identify genes that modulate treatment response to these drugs, we performed three genome-wide CRISPR/Cas9 knockout screens in the mCRPC cell line C4. The screens identified seven candidates for enzalutamide (BCL2L13, CEP135, E2F4, IP6K2, KDM6A, SMS, and XPO4), four candidates for docetaxel (DRG1, LMO7, NCOA2, and ZNF268), and nine candidates for cabazitaxel (ARHGAP11B, DRG1, FKBP5, FRYL, PRKAB1, RP2, SMPD2, TCEA2, and ZNF585B). We generated single-gene C4 knockout clones/populations for all genes and could validate effect on treatment response for five genes (IP6K2, XPO4, DRG1, PRKAB1, and RP2). Altered enzalutamide response upon IP6K2 and XPO4 knockout was associated with deregulation of AR, mTORC1, and E2F signaling, and deregulated p53 signaling (IP6K2 only) in C4 mCRPC cells. Our study highlights the necessity of performing individual validation of candidate hits from genome-wide CRISPR screens. Further studies are needed to assess the generalizability and translational potential of these findings. - Source: PubMed
Publication date: 2023/06/03
Haldrup JakobWeiss SimoneSchmidt LinnéaSørensen Karina Dalsgaard - Although an increasing number of common variants contributing to Alzheimer's disease (AD) are uncovered by genome-wide association studies, they can only explain less than half of the heritability of AD. Rare variant association studies (RVAS) has become an increasingly important area to explain the risk or trait variability of AD. - Source: PubMed
Publication date: 2022/05/07
Xiong WeixueCai JiahuiLi RuijiaWen CanhongTan HaizhuOn Behalf Of The Alzheimer's Disease Neuroimaging Initiative Adni Database