HBV Seroconversion Pane Donor# 71782
- Known as:
- Hepatitis B virus Seroconversion Pane Donor# 71782
- Catalog number:
- GENHBV11064
- Product Quantity:
- 9 specimens 1 mL)
- Category:
- -
- Supplier:
- Bio-gentaur
- Gene target:
- HBV Seroconversion Pane Donor# 71782
Related genes to: HBV Seroconversion Pane Donor# 71782
- Gene:
- CENPM NIH gene
- Name:
- centromere protein M
- Previous symbol:
- C22orf18
- Synonyms:
- Pane1, CENP-M, MGC861
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-03
- Date modifiied:
- 2014-11-18
Related products to: HBV Seroconversion Pane Donor# 71782
Related articles to: HBV Seroconversion Pane Donor# 71782
- - Source: PubMed
Publication date: 2025/08/16
Tang JinyuanZhang SihangJiang YongshuaiZhang Mingming - Centromere protein M (CENPM) promotes oncogenesis and serves as a prognostic biomarker in some cancers, but its implication in cutaneous melanoma is not clear. This study aimed to investigate the effect of targeting CENPM on cell proliferation, colony ability, apoptosis, invasion, migration, and BRAF inhibitor sensitivity, and its modification on Wnt/β-catenin, AKT, and P53 pathways in cutaneous melanoma. Cutaneous melanoma cell lines (A375 and SK-MEL-28) were transfected by CENPM siRNA (si-CENPM), followed by detections and treatment of various concentrations of dabrafenib and vemurafenib. Afterwards, 740Y-P (AKT activator) was added with or without si-CENPM transfection followed by detections. Gene Expression Profiling Interactive Analysis (GEPIA) public database was applied for clinical analysis. si-CENPM reduced cell proliferation, invasive cells and cell migration rate, but induced cell apoptosis rate in A375 and SK-MEL-28 cells. Meanwhile, si-CENPM decreased colony ability in A375 cells but didn't change colony ability in SK-MEL-28 cells. However, si-CENPM did not change cell viability under each concentration or IC value of BRAF inhibitors (dabrafenib and vemurafenib) in A375 and SK-MEL-28 cells. Interestingly, si-CENPM inactivated AKT pathway but less affected Wnt/β-catenin and P53 pathways in A375 and SK-MEL-28 cells. Afterwards, 740Y-P treatment attenuated the effect of si-CENPM on most of the above cellular functions in A375 and SK-MEL-28 cells. Clinically, GEPIA database revealed that CENPM was upregulated and correlated with worse overall survival in cutaneous melanoma patients. Targeting CENPM suppresses cutaneous melanoma growth and mobility by inactivating AKT pathway, indicating its potential as a treatment target. - Source: PubMed
Publication date: 2025/12/01
Ruan ShujieZhu ZhechenLuo BinlinTang YouzhiYan WeiShi Jingping - Glioma, one of the most common types of primary brain tumors, presents considerable challenges due to its poor prognosis. Emerging research has demonstrated a strong connection between Centromere Protein M(CENPM) and tumor progression. However, the precise role of CENPM in glioma remains poorly understood. This study delves into the involvement of CENPM in glioma progression. Data analysis revealed that heightened CENPM expression correlates with worse patient outcomes and is highly expressed in glioma. In vitro experiments showed that reducing CENPM expression inhibits glioma cell proliferation and induces G0/G1 phase cell cycle arrest. Furthermore, RNA-seq and Western Blot analyses demonstrated that CENPM activates the PI3K/AKT signaling pathway in glioma cells. In vivo experiments confirmed that knocking down CENPM leads to reduced tumor growth in glioma models and improves the prognosis of tumor-bearing mice. This study underscores the critical role of CENPM in glioma and sheds light on potential therapeutic strategies. - Source: PubMed
Publication date: 2025/11/27
Chen JiaweiTang FanBao SichenGao ZhuqiChen HongZhuge QichuanYang JianjingZhang Ying - Centromere protein M (CENPM), a member of the CENP family, is correlated with several malignancies, but its role in colon adenocarcinoma (COAD) is unclear. This study aims to explore the expression, prognostic significance, and biological role of CENPM in COAD. - Source: PubMed
Publication date: 2025/08/26
Cai ZhimingYang ZhenrongYu QianLin TaoSu XinchengLin LvZhou Yongjian - While normal cells are highly regulated, cancer cells take a dysregulated path which bolsters their survival. Currently, a limited number of uniform treatments are available for cancer cure. Our goal was to deprive cancer cells of the key nutrient methionine and determine what effect it would have on cell death and alterations in DNA methylation of prostate cancer cells. - Source: PubMed
Ramesh Babu Yatin SrinivashVenkatachalam Kallidaikurichi V