Ask about this productRelated genes to: CENPH Blocking Peptide
- Gene:
- CENPH NIH gene
- Name:
- centromere protein H
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-30
- Date modifiied:
- 2016-10-05
Related products to: CENPH Blocking Peptide
Related articles to: CENPH Blocking Peptide
- Climate change impacts the physiological processes of species, with rising seawater temperatures posing severe existential threats to marine mollusks. Therefore, studying the responses of marine organisms to heat stress is crucial. The blood clam, Anadara granosa, is a marine bivalve species that contains hemoglobin, and individuals with higher hemoglobin concentrations (HCs) exhibit better physiological health. In this study, we analyzed the regulatory mechanisms in the blood clam with different HCs in response to heat stress. Enzyme activity indicates that blood clams with different HC levels respond to heat stress by regulating oxidative stress and altering metabolic pathways, with clams with higher HCs showing greater adaptability and stress resistance. Transcriptome analysis of the control group (C), the high-HC heat-stressed group (TH), and the low-HC heat-stressed group (TL) revealed that endoplasmic reticulum processing and cytochrome P450 metabolism are crucial for the heat stress response. Additionally, the IP3R/Ca signaling pathway regulates the response in clams with higher HCs. Combined miRNA-mRNA analysis showed that clams with higher HCs have more heat-responsive genes, forming a more complex regulatory network. Dual-luciferase reporter assays revealed that agr-miR-936 negatively regulates Calr, involved in the heat stress response, while agr-miR-1935-Cenph may affect HC differences by regulating total hemocyte counts. Our findings deepen the understanding of the molecular regulatory mechanisms that allow blood clams to cope with heat stress, offering new insights for aquaculture to manage extreme temperatures amid global warming. - Source: PubMed
Publication date: 2026/07/21
He XinGuan XiaohuiShao JunfaBao Yongbo - Gallbladder stone (GS) and cholangiocarcinoma (CHOL) are common biliary tract disorders that share certain clinical and pathological characteristics but exhibit distinct molecular hallmarks. While GS-related inflammation, cholestasis, and epithelial injury-repair responses may provide a biologically plausible link, the shared genetic mechanisms underlying the pathogenesis of both diseases remain largely unexplored. The aim of this study was to elucidate this shared genetic landscape using a comparative transcriptomic approach. We identified 671 and 5197 differentially expressed genes (DEGs) in the GS and CHOL datasets, respectively. Gene ontology and KEGG enrichment analysis of these DEGs revealed possible involvement in IL-17 signaling and bile acid metabolism. The overlap of the DEGs yielded 15 common genes, which were further refined to three core genes-CENPH, NRSN2, and SPDYC-using LASSO regression analysis. The expression levels of these core genes were validated across multiple datasets, and ROC analysis demonstrated that they exhibited robust diagnostic performance for distinguishing both GS and CHOL. The copy number variations and promoter methylation status of these core genes were also evaluated. Candidate drug compounds targeting these genes were predicted using the PubChem database, and a gene-compound interaction network was constructed to facilitate future therapeutic investigations. We further confirmed that CENPH was significantly upregulated in CHOL cell lines (HuCC-T1 and RBE) compared to normal human intrahepatic biliary epithelial cells. Subsequently, loss-of-function assays showed that CENPH was essential for the proliferation, migration, and invasion of CHOL cells. In conclusion, our findings provide new insights into the shared genetic regulators of GS and CHOL and highlight the potential for developing effective diagnostic tools and tailored therapeutic strategies. - Source: PubMed
Publication date: 2026/07/06
Zhu ChenHuang KaigeZhang XiaohuiShi WeiweiFang JianHu SenyanZhang JiataoJiang HongboXie DongdongXu LiangmingSun YingCheng WentingKong XueyingYang XiaohuXu Dong - Oxidative stress correlates with the development and prognosis of lung adenocarcinoma (LUAD). This study, on the basis of oxidative stress-related genes (OSRGs), commences to identify molecular subtypes and develop prognostic model for LUAD. - Source: PubMed
Publication date: 2026/03/19
Zhang WeiranZhao XiaojiangWang YuhangLi Xin - Oocyte and early embryo competence defects (OECD) represent a recently recognized cause of female infertility with the application of assisted reproductive technology, characterized by impaired oocyte or early embryo development. To investigate the genetic landscape and subtypes of OECD, we performed whole-exome sequencing on 2,140 patients, classifying them into six distinct subtypes. We identified 183 pathogenic/likely pathogenic variants across 28 established genes. Notably, distinct genetic profiles and diagnostic rates emerged across subtypes, with a rate of 53% in the Empty Follicle subtype. Additionally, we identified and validated two potentially causative genes, MLH3 and CENPH. Gene burden analysis, using 2,424 fertile controls, suggested nine potential previously unreported associated genes and offered biological insights into the underlying pathogenic mechanisms of OECD. Collectively, these genetic findings accounted for 12.8-23.1% of OECD cases. This study delineates the genetic architecture of OECD, offering insights that may inform the development of diagnostic genetic screenings and provide a reference for standardized subtyping of patients with OECD. - Source: PubMed
Publication date: 2025/10/16
Zhang ChanglongZheng WeiZhang HonghuiZhao ShuaiHu HuilingXu XilinWan XianSun JiaqiSu WeiWang YangCui YingYang BohanYin ChangjianZhang XinLi ChengZhang XinZhang ChangmingWang ZhaoYuan YingLiu LiuMeng FeiZhang JiangtaoCao YongzhiGao YuanZhao ShigangGong FeiWu KeliangZhang FengTang ShuyanLin GeZhao HanChen Zi-Jiang - Centromere protein H (CENP-H) is an important component of a functional centromere. Studies have demonstrated that CENP-H is overexpressed in renal cell, gastric, hypopharyngeal squamous cell, nasopharyngeal, endometrial, lung, cervical, esophageal, liver, colorectal, oral squamous cell, breast, and tongue carcinomas. CENP-H overexpression is positively correlated with a poor prognosis, pathological stage, T stage, and lymph node metastasis in patients with the above carcinomas. CENP-H can promote cancer growth and metastasis through PI3K/AKT, survivin, and mitochondrial apoptosis signaling mechanisms, and it can be regulated by long non-coding ribonucleic acid (lncRNA) plasmacytoma variant translocation 1 (PVT1)/miR-612, Sp1, or Sp3. This review aims to summarize the expression of CENP-H, the relationship between CENP-H expression and prognostic features, growth and metastasis of cancer in patients, as well as the mechanism of CENP-H in cancer. It also proposes a new candidate molecule for treating patients with cancer. - Source: PubMed
Publication date: 2025/02/25
Li QiaoTang YangZuo Jie-BinHan HaoTu Guang-XuChen Cheng