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
- The genetic contributions of the X chromosome to Alzheimer's disease (AD) remain poorly understood yet are expected to importantly shape sex differences in AD. We therefore performed large-scale X-chromosome-wide association studies (N=1,240,451), evaluating differential risk due to sex, *4, and escape from X-chromosome inactivation, finding most X-linked loci appear relevant to female-biased AD etiology. In evaluating genetic pleiotropy with hormonal, lipid, and brain imaging traits, we discovered X-linked AD loci converged on white matter traits, particularly in the anterior corona radiata and splenium of the corpus callosum. Through brain-centric functional genomics analyses, we then nominated candidate causal genes, including 5 that appeared highly robust. Notably, we found the escape gene decreases AD risk in *4 carriers likely through higher expression in excitatory neurons to counter tau-related neurodegeneration. Altogether, we provide an atlas of sex and *4-informed candidate X-linked AD risk loci, genes, and mechanisms that will guide future studies. - Source: PubMed
Publication date: 2026/05/06
Cook NoahZeng YoujieYang ChenyuJiang ZhiwenWang Ting-ChenLe Guen YannCody KarlyJohnson MatthewZhang RuiMerritt Victoria CHauger Richard L Koran Mary EllenMormino Elizabeth CGordon BrianDeCasien AlexAndrews SheaDumitrescu LoganArcher DerekHohman Timothy JPottier CyrilCruchaga CarlosSherva RichardLogue MarkNapolioni ValerioGreicius Michael DBelloy Michael E - Abnormal chromatin remodeling figures prominently in the progression and treatment of malignancies. However, the prognostic significance of chromatin remodeling-related genes (CRRGs) in hepatocellular carcinoma (HCC) has not been extensively examined. Therefore, this study aimed to identify prognostic genes associated with chromatin remodeling in HCC and to determine their prognostic significance. - Source: PubMed
Publication date: 2026/02/25
Zhou ChuangLi DingSun Lin - The ovarian aging can lead to infertility, increase risk of diabetes, heart disease, and other serious problems. Ferroptosis is involved in the aging of various tissues. However, the mechanism underlying the role of ferroptosis in natural ovarian aging remains unclear. Here, we revealed the role of ferroptosis in ovarian aging and explore the intervention strategies for ovarian aging. Transcriptome data suggested that ferroptosis may be involved in ovarian aging. Through iron ion detection, Prussian blue staining, immunohistochemistry (IHC) staining and western blot (WB), we further confirmed that ferroptosis occurs in aging ovaries. Meanwhile, Acyl-CoA synthetase long-chain family member 4 (Acsl4) is highly expressed in senescent ovaries. We also found that the ferroptosis inhibitor Deferoxamine (DFO), Ferrostatin-1 (Fer-1) or the Acsl4 inhibitor Rosiglitazone (Rosi) inhibited ovarian aging and granulosa cell damage in vivo and in vitro. Further mechanistic studies have shown that Myeloid ectopic viral integration site 2 (Meis2) could cooperate with specificity protein 1 (SP1) to promote transcription of Acsl4 gene. Acetyl-proteomic analysis demonstrated that the acetylation level of K401 residue in Acsl4 (Acsl4-K401) was significantly reduced, and retinoblastoma binding protein 7 (Rbbp7) was identified via immunoprecipitation-mass spectrometry (IP-MS) as a direct mediator of Acsl4 deacetylation. Deacetylation of Acsl4-K401 can increase enzyme activity by promoting ATP binding. In conclusion, the increased expression level and the decreased acetylation level of Acsl4 protein promote ferroptosis, which in turn induces ovarian aging. Inhibiting ferroptosis or Acsl4 can alleviate ovarian aging. Our research has revealed a new mechanism of ovarian aging and provided potential new targets for alleviating it. - Source: PubMed
Publication date: 2025/12/30
Chen HongxuWang SiyuanDing ZhimingZhang NieLi JiaoyuZhang RuixinLiu XiaoyingXiang HuifenCheng LinghuiZhong FeiZhu Fengyu - Direct reprogramming of fibroblasts into cardiomyocytes by overexpressing cardiac transcription factors Gata4, Mef2c, and Tbx5 (GMT) is a promising way for cardiac repair, however, the low reprogramming efficiency remains a significant challenge. Cellular senescence, an irreversible cell-cycle arrest occurring in mitotic cells, has been reported to influence the efficiency of induced pluripotent stem cell (iPSC) reprogramming. - Source: PubMed
Publication date: 2025/12/29
Fang JuntaoYang QiangbingMaas Renée G CVader PieterMokry Michalvan den Dungen Noortje A MQian LiXiao JunjieSchiffelers RaymondLei ZhiyongSluijter Joost P G - Sepsis arises from a dysregulated host response to infection, leading to multiorgan inflammatory injury. Early diagnosis and treatment necessitate the identification of reliable immune biomarkers. This study investigated the relationship between aging, immunity, and sepsis by analyzing six human aging-related gene sets (656 genes). We identified 16 aging-related differentially expressed genes (DEGs) in sepsis. Among these, ATP11B, RBBP7, DOCK10, and NUP160 demonstrated the strongest connectivity with other genes and exhibited significant predictive power. Functional enrichment analysis (GO and KEGG) revealed distinct signaling pathway profiles between high-risk and low-risk sepsis groups (stratified based on risk scores). These dysregulated pathways, associated with multiple immune cells, were primarily linked to transcriptional dysregulation in cellular processes and cancer-related pathways. Experimental validation assays corroborated the roles of ATP11B and RBBP7. Collectively, our bioinformatic and experimental findings indicate that ATP11B, RBBP7, DOCK10, and NUP160 are implicated in the pathogenesis and progression of sepsis. But their potential for sepsis biomarkers still requires further verification. - Source: PubMed
Publication date: 2025/12/04
Sun XueyiGeng ShaoleiWang ZeyuanChen Qingjiang