Ask about this productRelated genes to: RBBP4 antibody
- Gene:
- RBBP4 NIH gene
- Name:
- RB binding protein 4, chromatin remodeling factor
- Previous symbol:
- -
- Synonyms:
- RbAp48, NURF55, lin-53
- Chromosome:
- 1p35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-05
- Date modifiied:
- 2016-05-25
Related products to: RBBP4 antibody
Related articles to: RBBP4 antibody
- Histone Deacetylase (HDAC) 1 and 2 are key enzymatic components in multiple large chromatin remodeling complexes including NuRD, SIN3, and CoREST. In addition, both HDAC 1 and 2 contain a large intrinsically disordered region (IDR) within their C-terminal domain (CTD). How HDAC1/2 assemble into these complexes and the structure of the CTD IDR remains poorly understood. Here, we used HDAC1/2 to isolate their protein interaction networks from cells and used crosslinking mass spectrometry (XL-MS) coupled with the Integrative Modeling Platform to build structural models of the NuRD, SIN3A, and CoREST complexes. Next, we implemented an AlphaFold-enabled XL-MS constrained modeling approach to investigate how HDAC1 could assemble into these complexes. We show that the CTD IDR of HDAC1 folds into alpha helices in these complexes. Finally, we built a complete integrative structural model of a NuRD subcomplex including the abundant HDAC1:MBD3:MTA1:GATAD2B:RBBP4 subunits, which included 6 IDRs. The approaches used herein are broadly applicable for the study of protein complexes and protein interaction networks that can provide important insights into IDRs. - Source: PubMed
Publication date: 2026/03/25
Nde JulesMajila KartikZimmermann Rosalyn CKempf CassandraZhang YingCesare JosephThornton Janet LWorkman Jerry LFlorens LaurenceViswanath ShruthiWashburn Michael P - Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder that is linked to cardiovascular, metabolic, and neurocognitive complications. However, its diagnosis relies on polysomnography, which is complex and resource-intensive, leading to frequent underdiagnosis. Emerging evidence suggests that accelerated biological aging may contribute to OSA pathophysiology, but systematic assessments using biological age metrics are limited. - Source: PubMed
Publication date: 2026/03/18
Wang YixuanWang YuhanZhang QingfengXiong JialiZhou BeiniWang MengcanWu ShujuanHu Ke - Lung cancer is the leading cause of global cancer mortality, with treatment efficacy limited by high heterogeneity, drug resistance, and an immunosuppressive tumor microenvironment. Focusing primarily on non-small cell lung cancer (NSCLC), this review systematically analyzes eight key regulated cell death (RCD) pathways in lung cancer. These pathways are apoptosis, autophagy, necroptosis, ferroptosis, cuproptosis, pyroptosis, immunogenic cell death (ICD), and lysosome-dependent cell death (LDCD). Mechanistic dissection reveals complex crosstalk and a dynamic equilibrium among these pathways. For instance, apoptosis escape via EGFR/PI3K/Akt/mTOR signaling promotes survival, while autophagy exhibits a context-dependent dual role regulated by factors such as RBBP4 and the AURKA-CXCL5 axis. Importantly, several RCD pathways exert potent immunomodulatory functions. Necroptosis activates T cells by releasing damage-associated molecular patterns (DAMPs), while ferroptosis enhances NK cell cytotoxicity through GPX4 inactivation. Regarding therapeutic advances, synergistic strategies show promise, such as berberine with EGFR-TKIs inducing apoptosis via EGFR degradation, and (-)-Guaiol triggering ICD to synergize with PD-1/PD-L1 inhibitors. Novel inducers, including Auranofin (ferroptosis), TMEM100 agonists (necroptosis), and cuproptosis nanomedicines (e.g., DE-CuO NPs), demonstrate preclinical potential. Prognostic models based on RCD-related genes (e.g., LDCD signatures) can predict immune features and response to immune checkpoint inhibitors (ICIs). However, clinical translation faces bottlenecks, including intricate pathway crosstalk, difficulties in remodeling the immunosuppressive niche, low ICI response in EGFR-mutant patients, and a lack of standardized biomarkers and optimized delivery systems. Future research should prioritize coordinated targeting of multiple death pathways, utilize advanced computational tools integrated with multi-omics data to decipher RCD network complexity and optimize treatment prediction, and strengthen interdisciplinary translational efforts. Ultimately, a deep understanding of the RCD network paves the way for a paradigm shift toward precision therapy in lung cancer. - Source: PubMed
Publication date: 2026/02/18
Xue FangsuSun JiachengZhang JitaiShen Yuntian - 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 - When SARS-CoV-2 became regional epidemics, a substantial number of patients suffered from post-acute sequelae of COVID-19 (PASC, aka long COVID). Exploring the pathogenesis and especially the heterogenicity features of long COVID subgroups is of paramount importance for understanding its etiology. In this study, through integrative multi-omics analyses encompassing transcriptomics, proteomics, and metabolomics, long COVID patients exhibited overall elevated MAPK pathway activation, while patients who have recovered from long COVID showed down-regulation of this response. Long COVID heterogenicity is described by multi-omics distinct signatures for each subgroup. The Multisystemic (MULTI) symptom subgroup is characterized by enhanced glycerophospholipid and ether lipid metabolism, Neurological (NEU) by augmented glycoprotein synthesis metabolism, Cardio cerebral (CACRB) by increased pyruvate metabolism and suppressed macrophage polarization, Musculoskeletal + Systemic (MSK + SYST) by elevated glycerophospholipid metabolism, and Cardiopulmonary (CAPM) by inhibited NF-κB signaling pathways. ABHD17A, CSNK1D, PSME4 and SYVN1 were general long COVID combination biomarkers, while CRH (MULTI), FPGT (NEU), CBX6 (CACRB) and RBBP4 (CAPM) were selected as serum-specific subgroup proteins. Our study provides a commonly shared and distinct pathophysiological explanation underpinning PASC, paving the way for future diagnosis and therapeutic interventions. - Source: PubMed
Publication date: 2024/11/15
Ai JingwenGuo JingxinLin KeCai JianpengZhang HaochengZhu FengSun GangqiangXue QuanlinZhu KunYang YixuanYuan GuanminSong JieyuFu ZhangfanQi XiaoSun YuhanLin WeifangQiu ChaoJiang NingWang SenZhang Wenhong