Ask about this productRelated genes to: CENPA antibody
- Gene:
- CENPA NIH gene
- Name:
- centromere protein A
- Previous symbol:
- -
- Synonyms:
- CENP-A, CenH3
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-31
- Date modifiied:
- 2014-11-19
Related products to: CENPA antibody
Related articles to: CENPA antibody
- Patients with systemic lupus erythematosus (SLE) exhibit elevated malignancy risk, with increased bladder cancer incidence. This study integrated Mendelian randomization (MR) with single-cell sequencing (scRNA-seq) to nominate exploratory prioritized candidate genes in SLE-bladder cancer comorbidity and their T cell regulatory roles. Single-cell datasets for SLE (GSE266852) and bladder cancer (GSE222315) were retrieved from GEO. Quality control, clustering, and annotation were performed using Seurat. T cell differentially expressed genes were intersected for bidirectional two-sample MR using IEU Open GWAS statistics. Heterogeneity, pleiotropy, and sensitivity analyses assessed robustness. GeneMANIA, miRNA databases, and CTD were used for network and functional analyses. Wilcoxon tests and Monocle 2 were used to characterize expression and T cell differentiation trajectories. Cross-disease intersection nominated 1010 candidate genes. In an exploratory MR screen (uncorrected < 0.05), four candidate genes were nominated (GBP3, LMAN1, SLC40A1, MIS18BP1); none survived FDR correction in both directions. At the uncorrected threshold, LMAN1 showed a shared risk direction (OR > 1) and MIS18BP1 a protective direction (OR < 1). Both showed significant T cell differential expression ( < 0.001) and elevated late differentiation expression. LMAN1 was involved in COPII vesicle transport; MIS18BP1 in CENP-A chromatin assembly. Twenty high-confidence miRNAs targeted each gene. CTD indicated liver injury associations and cisplatin/cyclosporine interactions. LMAN1 and MIS18BP1 are proposed as hypothesis-generating exploratory candidate genes in SLE-bladder cancer comorbidity, potentially involved in immune dysregulation through T cell terminal differentiation modulation. This study provides preliminary evidence suggestive of autoimmune-malignancy comorbidity mechanisms. - Source: PubMed
Publication date: 2026/08/21
Zhang DeshengRen HuanBai YunjinHan Ping - Centromeres are chromosomal loci required for accurate chromosome segregation in cell division and are defined epigenetically by the centromere-specific histone H3 variant CENP-A. The assembly and maintenance of CENP-A in each cell cycle are critical for continued centromere identity and function. In the germline, centromere identity must be maintained throughout many specialized divisions and preserved in gametes to ensure transgenerational inheritance. The male germline poses a particular challenge for maintaining centromere identity because most histones are removed from sperm chromatin and replaced by protamines in most animal species, causing a potential identity crisis. Here, we discuss the timing and mechanisms of centromere assembly and maintenance throughout spermatogenesis and the impacts on fertility and offspring development. We focus on , which has served as an informative model of the male germline, but also draw comparisons with other species, highlighting any conservation or adaptations. Finally, we outline unanswered questions in the field, identify technical barriers, and propose potential solutions. - Source: PubMed
Publication date: 2026/08/25
Ní Nualláin AnnaO'Gorman Ben DDunleavy Elaine M - The mammalian kinetochore connects chromosomes to dynamic spindle microtubules. To remain attached, it must maintain structural integrity under force, but to what extent and how it does so remain unclear. Under spindle forces, we find using super-resolution microscopy that inner (CENP-A) and outer (Hec1) metaphase kinetochores undergo correlated, large-scale (1 µm) deformations along the force axis, suggesting dynamic, relative sliding of parallel protein linkages. Kinetochore shape changes can be asymmetric, with centromere-facing "tails" correlating with hyperstabilized microtubule attachments. Applying microneedle pulling forces, we demonstrate that kinetochores are elastic, stretching under force and relaxing in seconds afterward. Finally, we show that SMC2 depletion results in more variable kinetochore deformations, despite maintained elasticity, and in reduced microtubule attachment stability. Thus, the kinetochore is structurally highly dynamic, requiring a stable centromere base to maintain structure and function under force. We propose a model whereby individual protein linkages are stiff, yet global kinetochore structure is flexible to accommodate different attachment geometries and forces while maintaining function. - Source: PubMed
Publication date: 2026/08/25
Tran Vanna MTao JinghuiRux Caleb JGomez Siu DavidRosas-Salvans MiquelDumont Sophie - Faithful chromosome segregation requires the kinetochore, a macromolecular protein complex that assembles on centromeric chromatin. In vertebrates, centromere identity is epigenetically defined by the histone H3 variant CENP-A, whose nucleosomes are replenished during early G1 phase through a cell cycle-regulated deposition mechanism. The CENP-A chaperone HJURP is recruited to centromeres via the Mis18 complex to enable CENP-A incorporation (Mis18C pathway). Recent genetic analyses in chicken cells, however, revealed an additional, independent recruitment route via direct HJURP-CENP-C interaction (CENP-C pathway). Structural studies show that CENP-C and the Mis18C subunit KNL2/M18BP1 engage pre-existing CENP-A nucleosomes at different surfaces of the Constitutive Centromere-Associated Network (CCAN), constraining the spatial coordinates where new CENP-A is incorporated. This review summarizes current understanding of HJURP recruitment mechanisms for vertebrate CENP-A deposition and proposes that this structure-defined deposition geometry underlies epigenetic self-propagation of centromere positional information by maintaining proper CCAN spacing across cell divisions. - Source: PubMed
Hori TetsuyaFukagawa Tatsuo - Ewing sarcoma (EwS) is characterized by chimeric fusions such as EWSR1::FLI1. Chromosome gain or loss is prevalent in EwS, and this chromosome instability (CIN) phenotype correlates with poor treatment outcomes. We previously showed that CENP-A, a centromere-specific histone H3 variant, interacts with EWSR1 via its SYGQ2 motif, an interaction extending to the EWSR1::FLI1 fusion protein. CENP-A is highly expressed in EwS cells, driven by EWSR1::FLI1. EwS cells exhibit significant CIN, mitigated by depleting EWSR1::FLI1 or CENP-A, and frequently assemble neocentromeres. Using CENP-A ChIP-seq, we identify neocentromere-associated DNA sequences, and ChIP assays confirm EWSR1::FLI1 binds these sequences, suggesting EWSR1::FLI1 recruits CENP-A to drive neocentromere assembly. Notably, overexpressing EWSR1::FLI1, but not CENP-A, induces neocentromeres in non-EwS cells. These neocentromeres likely produce dicentric chromosomes, explaining the high incidence of chromosome bridges and chromoplexy underlying the CIN phenotype in EwS. - Source: PubMed
Publication date: 2026/08/14
Kitagawa RisaMetitiri Ediri EYu BinShen ChangxianBishop Alexander J RZheng SiyuanHoughton Peter JKitagawa Katsumi