Mouse AntiCENPE Target Antigen CENPE Host Isotype Mouse IgG1_ Application ICC; IF; IP; WB (after antigen concentration);
- Known as:
- Mouse AntiCENPE Target Antigen CENPE Host Isotype Mouse IgG1_ Application ICC; IF; IP; Western Blot (after antigenic concentration);
- Catalog number:
- IQ254
- Product Quantity:
- 50ul (0.45mg/ml)
- Category:
- -
- Supplier:
- Imunquest
- Gene target:
- Mouse AntiCENPE Target Antigen CENPE Host Isotype IgG1_ Application ICC; ; (after antigen concentration);
Related genes to: Mouse AntiCENPE Target Antigen CENPE Host Isotype Mouse IgG1_ Application ICC; IF; IP; WB (after antigen concentration);
- Gene:
- CENPE NIH gene
- Name:
- centromere protein E
- Previous symbol:
- -
- Synonyms:
- KIF10, PPP1R61
- Chromosome:
- 4q24
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-04
- Date modifiied:
- 2016-10-05
- Gene:
- PRRT2 NIH gene
- Name:
- proline rich transmembrane protein 2
- Previous symbol:
- ICCA, DYT10
- Synonyms:
- FLJ25513, DKFZp547J199, IFITMD1, FICCA, DSPB3, PKC, EKD1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-25
- Date modifiied:
- 2018-03-19
- Gene:
- SCN5A NIH gene
- Name:
- sodium voltage-gated channel alpha subunit 5
- Previous symbol:
- CMD1E
- Synonyms:
- Nav1.5, LQT3, HB1, HBBD, PFHB1, IVF, HB2, HH1, SSS1, CDCD2, CMPD2, ICCD
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-10
- Date modifiied:
- 2019-04-23
Related products to: Mouse AntiCENPE Target Antigen CENPE Host Isotype Mouse IgG1_ Application ICC; IF; IP; WB (after antigen concentration);
Related articles to: Mouse AntiCENPE Target Antigen CENPE Host Isotype Mouse IgG1_ Application ICC; IF; IP; WB (after antigen concentration);
- Castration-resistant prostate cancer (CRPC) progression despite treatment with potent androgen receptor (AR) antagonists such as enzalutamide is a major clinical challenge. The mitotic kinase BUB1B is a central member of an oncogenic seven-gene network that drives CRPC. Here, we characterized BUB1B as an actionable therapeutic target for treatment-resistant PC. High BUB1B expression correlated with PC progression and aggressiveness. BUB1B depletion blocked CRPC cell proliferation through accumulation in G2/M and mitotic delay. Conversely, ectopic expression of BUB1B conferred castration and enzalutamide resistance to androgen-dependent PC cells in vitro and in vivo. BUB1B promotion of CRPC was not dependent on AR canonical signaling as assessed through AR knockdown and PROTAC-mediated AR degradation. BUB1B kinase activity was necessary for CRPC progression, as only wild type (WT), but not two kinase-dead mutants, promoted castration-resistant growth, and BUB1B kinase activity was required to maintain castration resistance. Expression of the primary substrate of BUB1B, CENP-E, also promoted CRPC progression, while a phosphodeficient mutant of the BUB1B phosphorylation site was ineffective. Moreover, only a phosphomimic mutant of CENP-E rescued growth after BUB1B depletion in CRPC cells, indicating that BUB1B-dependent phosphorylation of CENP-E was sufficient for progression and necessary to sustain CRPC growth. Targeting CENP-E with the clinically tested, small-molecule GSK923295 phenocopied BUB1B knockdown, sensitized resistant cells to enzalutamide and suppressed growth of enzalutamide-resistant xenografts in vivo. These data support BUB1B kinase as a driver of castration and enzalutamide resistance, positioning CENP-E inhibition as an attainable approach for treatment-resistant disease. - Source: PubMed
Publication date: 2026/09/18
Martinez Maria JBlanco CynthiaPeinetti NahuelCooke MarianaLyles Rolando DzRevuelta Maria VCorey EvaStathias VasileiosCampbell Moray JBurnstein Kerry L - Accurate segregation of mitotic chromosomes requires pre-anaphase alignment driven by microtubule-based motor proteins. Tubulin detyrosination is essential to guide CENP-E-driven chromosome congression in mitosis. However, the mechanisms of action and physiochemical properties of the detyrosinases for decoding CENP-E motility remain elusive. Here we show that microtubule-associated tyrosine carboxypeptidase (MATCAP) undergoes intrinsically disordered region (IDR)-dependent liquid-liquid phase separation (LLPS) on microtubules to constitute the tubulin detyrosination machinery. These biomolecular condensates selectively enrich tubulin and CENP-E, thereby stabilizing kinetochore-microtubule attachments. Real-time imaging of cells expressing LLPS-deficient MATCAP mutants reveals the importance of MATCAP LLPS dynamics in mitotic chromosome alignment. Mechanistically, phase separation of MATCAP spatiotemporally couples tubulin detyrosination with CENP-E motility to ensure a robust chromosome alignment during mitosis. These findings delineate a signaling cascade that integrates phase separation and tubulin detyrosination with mitotic progression for the maintenance of genomic stability. - Source: PubMed
Publication date: 2026/07/30
Yang TongtongHu WenpingXu PanpanLi HuanyuZhang YaqianXiong FangyuanLi YunzeXu ChaoRuan KeHou ZhonghuaiWang ZhikaiZhang LiangyuYao XuebiaoXiang ShengqiJiang KaiLiu Xing - The prognostic role of molecular subtypes of prostate cancer (PCa) patients is still unclear. And we speculated whether the change of immunologic and hallmark gene sets of adjacent notumor tissues could promote the BCR of PCa patients. - Source: PubMed
Publication date: 2026/07/23
Lin YiweiZhou Jiatong - Oxidative stress and the tumor immune microenvironment jointly shape hepatocellular carcinoma (HCC) progression and response to immunotherapy, yet integrated biomarkers linking these processes are lacking. - Source: PubMed
Publication date: 2026/08/04
Liang YuxinChen XingSu YuhaoZhong DeyuanYan HongtaoChen YahuiWang MingYang QinyanHuang Xiaolun - High-linear energy transfer (LET) radiation such as carbon ions exhibits greater biological effectiveness than conventional low-LET X-rays, but the transcriptional mechanisms underlying this advantage remain incompletely understood. We hypothesized that high-LET radiation induces a qualitatively different transcriptional response rather than simply amplifying low-LET signaling. - Source: PubMed
Publication date: 2026/07/14
Nisar HasanSerçin ÖzdemirhanHellweg Christine E