Ask about this productRelated genes to: CENPB antibody
- Gene:
- CENPB NIH gene
- Name:
- centromere protein B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-31
- Date modifiied:
- 2015-11-05
Related products to: CENPB antibody
Related articles to: CENPB antibody
- While homologous recombination (HR) is often considered to be an error-free DNA repair mechanism, the fidelity of this pathway depends on the cell's ability to engage the ideal template: the replicated sister chromatid. This is particularly challenging during repair of repetitive genome regions for which nonallelic sequences can errantly be used as templates. We developed a model to study spontaneous DNA damage and repair that occurs at repetitive protein-coding genes of the flocculin family. We observed that genes encoding most members of this protein family constitutively reside at the nuclear periphery by virtue of their close proximity to binding sites for the CENP-B-like protein, Cbp1. Tethering via Cbp1 to the nuclear periphery enhances the stability of the flocculin genes against intragenic recombination and restrains intergenic recombination between homoeologous repeat-encoding sequences. The LINC complex component Kms1 also antagonizes both intragenic and intergenic recombination at the flocculin genes as well as microhomology-mediated end joining (MMEJ). Our observations suggest that leverages nuclear compartmentalization to maintain the stability of repetitive genic regions at the nuclear periphery, while association of DSBs with Kms1-containing LINC complexes enforces stringency to avoid mutagenic end joining and use of the incorrect template during HR. - Source: PubMed
Publication date: 2026/04/01
Laffitte AlyssaLin DongxuTian Yingzhen JennyLiu NaLusk C PatrickMochrie Simon G JKing Megan C - This study evaluates the consistency between the centromere AC-3 immunofluorescence pattern and the anti-centromere protein B (anti-CENP-B) antibody test results and analyzes differences in the positive rates of potential related diseases with anti-centromere antibody (ACA) positivity. A retrospective collection of antinuclear antibody fluorescent patterns and anti-CENP-B test data from inpatients at Maanshan People's Hospital between February 2022 and February 2024 was performed. The consistency of different methods was evaluated using the kappa test and overall consistency calculation. Subsequently, the main diagnostic information of patients with ACA positivity was extracted, and the positive rates of ACAs in potential related diseases were analyzed. A total of 7893 patients were tested for both antinuclear antibody patterns and anti-CENP-B antibodies. Among them, 3959 patients were tested for ACAs using indirect immunofluorescence and Western blotting; 3936 patients were tested by indirect immunofluorescence and multiplex flow cytometric immunoassay. The consistency analysis showed that the kappa coefficients for both comparisons were >0.81, and the overall consistency was >99%, indicating that the AC-3 pattern and anti-CENP-B antibody test results were almost completely consistent. ACA positivity was observed in a variety of autoimmune diseases, with systemic sclerosis showing the highest positive rate (41.18%, 95% confidence interval: 32.12%-50.88%), followed by primary biliary cholangitis (40.00%, 95% confidence interval: 11.76%-76.93%). The positive rates of ACAs in 16 diseases were significantly higher than those in healthy control populations. There was almost complete consistency between the AC-3 pattern and the anti-CENP-B antibody test, suggesting that CENP-B is the main target antigen of the AC-3 pattern. ACA positivity was observed in various autoimmune diseases, especially systemic sclerosis and primary biliary cholangitis. This study offered useful insights for both basic and clinical investigations of ACAs. - Source: PubMed
He SongWu YingKe Li-PingWu PingXu Da-Hai - Anti-centromere antibodies are associated with limited cutaneous systemic sclerosis (lcSSc) and a more favorable prognosis. The centromere HEp-2 pattern (AC-3) suggests the presence of antibodies against CENP antigens, mainly CENP-B/A. This study analyzed clinical and demographic associations of anti-centromere antibodies in a cohort of patients exclusively with the lcSSc form of SSc. The frequency of CENP-B and CENP-A reactivity in samples with the AC-3 pattern was also evaluated. - Source: PubMed
Publication date: 2025/11/26
Keppeke Gerson DLandoni DianaKayser CristianeMatos PedroDiogenes LarissaKeppeke JessicaRodrigues Silvia HelenaC Andrade Luis Eduardo - : Systemic sclerosis (SSc) is a heterogeneous connective tissue disease characterized by immune dysregulation, vasculopathy, and fibrosis. Objectives: To evaluate the genetic architecture and autoantibody profile in a Kazakh cohort of patients with SSc. : A total of 26 Kazakh patients with diffuse SSc were examined for disease activity and organ impairment using EScSG and the modified Rodnan skin score (mRSS). Eighteen healthy volunteers were enrolled in the control group. Antinuclear factor (ANF) was estimated on HEp-2 cells, while antibodies to Scl-70, CENP-B, U1-snRNP, SS-A/Ro52, SS-A/Ro60, Sm/RNP, Sm, SS-B, Rib-P0, and nucleosomes were determined by immunoblotting. The level of IL-6 cytokine was detected using ELISA. To investigate the genetic basis of SSc in Kazakh patients, a custom AmpliSeq panel including targeting immune/fibrosis pathways and 120 genes was used on the Ion Proton sequencer. The statistical analysis of categorical variables was conducted using Fisher's exact test and Chi-square (χ) test. : The examination of SSc patients (mRSS 16 ± 7.2; EScSG 3.54 ± 2.18) revealed a broad range of antibodies to Scl-70, CENP-B, SS-A/Ro60, SS-A/Ro52, U1-snRNP, and RNP/Sm, which were undetectable in the control group. Genetic analysis identified multiple variants across immune regulatory genes, including likely pathogenic changes in SAMD9L, REL, IL6ST, TNFAIP3, ITGA2, ABCC2, AIRE, IL6R, AFF3, and TREX1. Variants of uncertain clinical significance were detected in LY96, IRAK1, RBPJ, IL6ST, ITGA2, AIRE, IL6R, JAZF1, IKZF3, IL18, IL12B, PRKCQ, PXK, and DNASE1L3. Novel variants at the following genomic coordinates were identified and have not been previously reported in association with SSc: LY96 (chr8:74922341 CT/C), PTPN22 (chr1:114381166 CT/C), IRAK1 (indels at chrX:153278833), and SAMD9L (chr7:92761606 GT/G; chr7:92764981 T/TT). : The first immunogenetic investigation of SSc in Kazakhstan revealed a polygenic architecture involving immune signalling pathways that partially overlap with international cohorts while exhibiting region-specific variation. Although the limited sample size and lack of functional validation constrain the interpretability of the findings, the results provide a framework for larger research to confirm the pathogenic mechanisms and establish clinical relevance. - Source: PubMed
Publication date: 2025/10/28
Zaripova LinaBaigenzhin AbaiBoltanova AlyonaZhabakova ZhannaSolomadin MaximKozina Larissa - Centromere breakage has been associated with anti-centromere antibodies in systemic sclerosis (SSc), yet the origins of centromere damage and its link to immune activation remain unclear. The bleomycin induced fibrosis model is widely used as an experimental model of SSc. Here, we investigated whether bleomycin selectively disrupts centromeres and whether such damage contributes to chromosome instability and immunogenic chromatin mislocalization. - Source: PubMed
Publication date: 2025/12/04
Imtiaz AzaitWaseem MohammadO'Neill HudsonWright Christine MChen Bo-RueiCzaja WiolettaContreras-Galindo Rafael