Ask about this productRelated genes to: CCNB1IP1 antibody
- Gene:
- CCNB1IP1 NIH gene
- Name:
- cyclin B1 interacting protein 1
- Previous symbol:
- C14orf18
- Synonyms:
- HEI10
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-02
- Date modifiied:
- 2016-03-18
Related products to: CCNB1IP1 antibody
Related articles to: CCNB1IP1 antibody
- The leading cause of human pregnancy loss is aneuploidy, often tracing to errors in chromosome segregation during female meiosis. Although abnormal crossover recombination is known to confer risk for aneuploidy, limited data have hindered understanding of the potential shared genetic basis of these key molecular phenotypes. To address this gap, we performed retrospective analysis of pre-implantation genetic testing data from 139,416 in vitro fertilized embryos from 22,850 sets of biological parents. By tracing transmission of haplotypes, we identified 3,809,412 crossovers, as well as 92,485 aneuploid chromosomes. Counts of crossovers were lower in aneuploid versus euploid embryos, consistent with their role in chromosome pairing and segregation. Our analyses further revealed that a common haplotype spanning the meiotic cohesin SMC1B is associated significantly with both crossover count and maternal meiotic aneuploidy, with evidence supporting a non-coding cis-regulatory mechanism. Transcriptome- and phenome-wide association tests also implicated variation in the synaptonemal complex component C14orf39 and crossover-regulating ubiquitin ligases CCNB1IP1 and RNF212 in meiotic aneuploidy risk. More broadly, variants associated with aneuploidy often showed secondary associations with recombination, and several also exhibited associations with reproductive ageing traits. Our findings highlight the dual role of recombination in generating genetic diversity, while ensuring meiotic fidelity. - Source: PubMed
Publication date: 2026/01/21
Carioscia Sara ABiddanda ArjunStarostik Margaret RTang XiaonaHoffmann Eva RDemko Zachary PMcCoy Rajiv C - Colorectal cancer (CRC) is a leading cause of cancer mortality, with treatment resistance often driven by molecular heterogeneity and an immunosuppressive tumor microenvironment (TME). Post-translational modifications (PTMs) regulate key oncogenic processes, but their comprehensive role in CRC progression and immune evasion remains unexplored. - Source: PubMed
Publication date: 2025/09/26
Yang GuitingJi LiuLv ChengmeiZhao ChenMa RiliangLi YingHu YanyanPan Linghui - Olfactomedin 4 (OLFM4) is endogenously expressed in several normal human tissues and exerts its biological functions through its diverse binding partners on both the cell surface and intracellularly. OLFM4 is involved in multiple cellular functions, such as proliferation, apoptosis, and adhesion. OLFM4 is also a target gene in several important inflammation- and cancer-related pathways, and OLFM4 plays important roles in both infectious and inflammatory diseases and a variety of cancers. Studies of OLFM4 expression and function in cancer development and progression in numerous cancers indicate that OLFM4 exerts tumor-suppressing or tumor-promoting effects depending on the tissue and cellular context, and that OLFM4 is aberrantly expressed and functionally involved in multiple human cancers through different mechanisms. In cancers where OLFM4 is upregulated or plays a tumor-promoting role, therapies designed to inhibit OLFM4 expression may be clinically beneficial. OLFM4 could also have utility as a biomarker for early detection and diagnosis of precancerous states in several human cancers. - Source: PubMed
Publication date: 2025/08/18
Liu WenliRodgers Griffin P - Our earlier research identified FUBP1 as a promising biomarker for triple-negative breast cancer (TNBC). However, its role in RNA networks governing TNBC cell proliferation and invasion remains unclear. Here, we developed a stable MDA-MB-231 cell line with reduced FUBP1 expression and performed transcriptome sequencing. We found 1084 differentially expressed mRNAs, 2394 lncRNAs, and 497 circRNAs following FUBP1 knockdown. KEGG analysis showed enrichment in pathways like PI3K-Akt signaling and ECM receptor interaction. Notably, lnc-CCNB1IP1-1-1 was down-regulated upon FUBP1 knockdown, and its suppression inhibited cell proliferation, migration, and invasion. Additionally, lnc-CCNB1IP1-1-1 knockdown reduced PARP2 expression. Thus, FUBP1 knockdown activates lnc-CCNB1IP1-1-1 to modulate TNBC progression, revealing new insights into FUBP1's role in TNBC RNA networks. - Source: PubMed
Publication date: 2025/06/28
Liu WeiLiang PeideChen LihongLiang RongXiong Xifeng - The leading cause of human pregnancy loss is aneuploidy, often tracing to errors in chromosome segregation during female meiosis. While abnormal crossover recombination is known to confer risk for aneuploidy, limited data have hindered understanding of the potential shared genetic basis of these key molecular phenotypes. To address this gap, we performed retrospective analysis of preimplantation genetic testing data from 139,416 fertilized embryos from 22,850 sets of biological parents. By tracing transmission of haplotypes, we identified 3,656,198 crossovers, as well as 92,485 aneuploid chromosomes. Counts of crossovers were lower in aneuploid versus euploid embryos, consistent with their role in chromosome pairing and segregation. Our analyses further revealed that a common haplotype spanning the meiotic cohesin is significantly associated with both crossover count and maternal meiotic aneuploidy, with evidence supporting a non-coding -regulatory mechanism. Transcriptome- and phenome-wide association tests also implicated variation in the synaptonemal complex component and crossover-regulating ubiquitin ligases and in meiotic aneuploidy risk. More broadly, recombination and aneuploidy possess a partially shared genetic basis that also overlaps with reproductive aging traits. Our findings highlight the dual role of recombination in generating genetic diversity, while ensuring meiotic fidelity. - Source: PubMed
Publication date: 2025/04/04
Carioscia Sara ABiddanda ArjunStarostik Margaret RTang XiaonaHoffmann Eva RDemko Zachary PMcCoy Rajiv C