Ask about this productRelated genes to: RBBP7 antibody
- Gene:
- RBBP7 NIH gene
- Name:
- RB binding protein 7, chromatin remodeling factor
- Previous symbol:
- -
- Synonyms:
- RbAp46
- Chromosome:
- Xp22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-23
- Date modifiied:
- 2016-10-05
Related products to: RBBP7 antibody
Related articles to: RBBP7 antibody
- Centromeres are specialized chromosomal loci that ensure faithful chromosome segregation during mitosis, a function that depends on the precise localization of the histone H3 variant centromere protein A (CENP-A) within centromeric chromatin. CENP-A deposition is tightly regulated by assembly factors, including HJURP; however, the complete regulatory network remains incompletely defined. Using CENP-A immunoprecipitation coupled with mass spectrometry, we identified SET, a multifunctional chromatin-associated protein involved in transcription and nucleosome assembly, as one of the most enriched proteins in CENP-A immunoprecipitates, suggesting an association between SET and CENP-A. Here, we investigated this association and its functional significance. Reciprocal co-immunoprecipitation assays showed that SET associates with both CENP-A and HJURP. Immunofluorescence analysis revealed that SET localizes to centromeres and that SET depletion reduces centromeric CENP-A enrichment. Live-cell imaging further showed that SET depletion causes chromosome alignment defects and prolonged mitotic arrest. Together, these findings identify SET as a previously unrecognized regulator of the CENP-A-HJURP axis and suggest that SET supports proper CENP-A localization at centromeres and faithful mitotic progression. This study expands our understanding of the regulatory network that maintains centromere identity. - Source: PubMed
Wang YingHu ChengchengWang XinyangXiong FangyuanYao XuebiaoWang Zhikai - Identifying therapeutic protein targets is challenging due to unpredictable druggability. Exploring multi-purpose drug targetomes, such as that of rapamycin, offers a valuable strategy for target discovery. Here, using chemical proteomics, we identified the histone-binding protein RBBP7 as a previously unrecognized target of rapamycin. Rapamycin disrupts the RBBP7-H4 interaction, leading to reduced histone H4 acetylation and downregulation of DNMT1. Based on this mechanism, we designed RBBP7-targeting peptides (RBBP7-TPs). RBBP7-TP4 exhibited potent anti-tumor activity in both cellular and xenograft mouse models of hepatocellular carcinoma (HCC). Furthermore, RBBP7-TP4 synergized with HDAC inhibitors to enhance epigenetic efficacy in HCC models, supporting a promising combination strategy. Collectively, our findings highlight the value of mining multi-purpose drug targetomes for therapeutic target discovery. RBBP7 is established as a druggable target in cancer, and RBBP7-TP4 represents a potential peptide-based therapeutic candidate. - Source: PubMed
Publication date: 2026/09/15
Gao ZanSun LeLi JianlongLv HengYou YingnanWang KunSu NanWang LinLiu NanHu JunhaoJiang HongShan BingZhang Yaoyang - Asymmetric transcription of noncoding RNA LincGET is currently recognized as the earliest event regulating the first cell fate decision in mammalian embryogenesis. However, whether key protein factors modulate this process remains elusive. Here, we identify RBBP7 as the earliest protein factor regulating developmental cell fate in mammals. Loss of RBBP7 drives cells towards ICM lineage. In mouse late 2-cell embryos, unequal translation of Rbbp7 contributes to its asymmetric protein distribution, which subsequently induces inversed asymmetric histone acetylation H3K9ac by interaction with HDAC1, thereby promoting cell differentiation. Interestingly, RBBP7 and LincGET exhibit a consistent asymmetric tendency but direct different cell fates; depletion or overexpression of both Rbbp7 and LincGET restored the cell fate bias, suggesting a coordinated regulatory mechanism during initial lineage specification. In summary, our study reveals RBBP7 as a new protein factor and elucidates its role in the first cell fate decision. - Source: PubMed
Publication date: 2026/08/18
Ju Lin-FangHan XiaoZhang DanruXu Heng-JiJia ShaokangLiu Meng-XiaLiu YanchenCai Yu-TingChen Yu-ShengGao Chun-ChunZhao Yong-LiangHao YajingWang Xiu-JieLi DangshengZhou XiangYang YingHan JianyongYang Yun-Gui - Ovarian cancer (OC) remains one of the leading causes of gynecological cancer-related mortality, with limited biomarkers for early detection and prognosis. Changes in DNA methylation-stable and detectable in blood-are potential candidates for clinical application. In our earlier genome-wide methylation study involving monozygotic twins where one had ovarian cancer and the other did not, we identified two genes, RBBP7 and RIBC1, as differentially methylated. These findings laid the groundwork for further targeted investigation. - Source: PubMed
Publication date: 2026/07/29
Erdoğan Özge ŞükrüoğluErciyas Seda KılıçDemirbaş Betül ÇelikDinç AhmetÜnal ElifUğurlucan Funda GüngörÖdemiş Demet AkdenizPasin ÖzgeSaip Pınar MuallaYazıcı HülyaTuncer Seref Bugra - Polycomb repressive complex 2 (PRC2) silences MHC class I antigen presentation across cancer types, yet the role of its core scaffolding subunit SUZ12 in pancreatic ductal adenocarcinoma (PDAC) immune phenotypes remains poorly characterized. - Source: PubMed
Publication date: 2026/06/23
Wang ZhuoxinJin ChenyangYin FeiWu XuejiaoYang Zilin