RBBP7

Last update 08 May 2025

Basic Info

Synonyms

Histone acetyltransferase type B subunit 2, Histone-binding protein RBBP7, Nucleosome-remodeling factor subunit RBAP46

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Introduction

Core histone-binding subunit that may target chromatin remodeling factors, histone acetyltransferases and histone deacetylases to their histone substrates in a manner that is regulated by nucleosomal DNA. Component of several complexes which regulate chromatin metabolism. These include the type B histone acetyltransferase (HAT) complex, which is required for chromatin assembly following DNA replication; the core histone deacetylase (HDAC) complex, which promotes histone deacetylation and consequent transcriptional repression; the nucleosome remodeling and histone deacetylase complex (the NuRD complex), which promotes transcriptional repression by histone deacetylation and nucleosome remodeling; and the PRC2/EED-EZH2 complex, which promotes repression of homeotic genes during development; and the NURF (nucleosome remodeling factor) complex.

100 Clinical Results associated with RBBP7

100 Translational Medicine associated with RBBP7

0 Patents (Medical) associated with RBBP7

146

Literatures (Medical) associated with RBBP7

01 Mar 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

IKZF1 promotes pyroptosis and prevents M2 macrophage polarization by inhibiting JAK2/STAT5 pathway in colon cancer

Article

Author: Lin, Bingheng ; Zhang, Renyi ; Zhu, Huacong ; Huang, Kaihua ; Dong, Xiaoyu ; Lin, Jiabao ; Zheng, Ruinian ; Jing, Fangyan ; Zhu, Yu ; Li, Shenglong ; Liu, Guanglong ; Wu, Chaosong ; Bao, Ming

Pyroptosis and macrophage pro-inflammatory activation play an important role in hepatocellular carcinoma (HCC) progression. However, the specific regulatory mechanisms remain unclear. We identified pyroptosis-related differentially expressed genes (DEGs) based on the GSE4183 and GSE44861 datasets as well as EVenn database. Expression levels of key genes were detected by qRT-PCR. IKZF1 was overexpressed in colon cancer cells and tumor-bearing mice, and its functions were assessed by various cell biology assays in vitro and in vivo. To investigate the interactions between IKZF1 and macrophages, a co-culture system was constructed. The activator RO8191 or inhibitor ruxolitinib of the JAK/STAT pathway was employed to confirm whether IKZF1 inhibited colon cancer development by regulating JAK2/STAT5 pathway. Pyroptosis-related hub genes RBBP7, HSP90AB1, and RBBP4 were highly expressed, while IKZF1, NLRP1, and PYCARD were lowly expressed. These hub genes had good performance in distinguishing colon cancer from controls. Furthermore, overexpression of IKZF1 inhibited tumor growth and promoted pyroptosis. Overexpression of IKZF1 suppressed cell proliferation, metastasis, and inactivated JAK2/STAT5 signaling pathway in colon cancer cells. Furthermore, upregulation of IKZF1 promoted M1 macrophage polarization while inhibiting M2 macrophage polarization in vivo and in vitro by inhibiting the JAK2/STAT5 signaling pathway. This study identifies IKZF1 as a potential biomarker inactivating JAK2/STAT5 pathway for colon cancer.

31 Dec 2023·Cell journal

Integrated Bioinformatic Analysis of Differentially Expressed Genes Associated with Wound Healing.

Article

Author: Samadikuchaksaraei, Ali ; Farhangniya, Mansoureh ; Salehi, Najmeh ; Mohamadi Farsani, Farzaneh

OBJECTIVEWound healing is a complex process involving the coordinated interaction of various genes and molecular
pathways. The study aimed to uncover novel therapeutic targets, biomarkers and candidate genes for drug development
to improve successful wound repair interventions.
Materials and Methods: This study is a network-meta analysis study. Nine wound healing microarray datasets obtained
from the Gene Expression Omnibus (GEO) database were used for this study. Differentially expressed genes (DEGs)
were described using the Limma package and shared genes were used as input for weighted gene co-expression
network analysis. The Gene Ontology analysis was performed using the EnrichR web server, and construction of a
protein-protein interaction (PPI) network was achieved by the STRING and Cytoscape.
Results: A total of 424 DEGs were determined. A co-expression network was constructed using 7692 shared genes
between nine data sets, resulting in the identification of seven modules. Among these modules, those with the top 20
genes of up and down-regulation were selected. The top down-regulated genes, including TJP1, SEC61A1, PLEK,
ATP5B, PDIA6, PIK3R1, SRGN, SDC2, and RBBP7, and the top up-regulated genes including RPS27A, EEF1A1,
HNRNPA1, CTNNB1, POLR2A, CFL1, CSNk1E, HSPD1, FN1, and AURKB, which can potentially serve as therapeutic
targets were identified. The KEGG pathway analysis found that the majority of the genes are enriched in the "Wnt
signaling pathway".
Conclusion: In our study of nine wound healing microarray datasets, we identified DEGs and co-expressed modules
using WGCNA. These genes are involved in important cellular processes such as transcription, translation, and posttranslational
modifications. We found nine down-regulated genes and ten up-regulated genes, which could serve as
potential therapeutic targets for further experimental validation. Targeting pathways related to protein synthesis and cell
adhesion and migration may enhance wound healing, but additional experimental validation is needed to confirm the
effectiveness and safety of targeted interventions.

16 Oct 2023·The Journal of clinical investigation

X-linked RBBP7 mutation causes maturation arrest and testicular tumors.

Article

Author: Yang, Xiaohang ; Li, Jingping ; Hou, Jiaru ; Jin, Fan ; Zheng, Huimei ; Zhang, Fengbin ; Xi, Yongmei ; Chen, Jianhua

Maturation arrest (MA) is a subtype of non-obstructive azoospermia, and male infertility is a known risk factor for testicular tumors. However, the genetic basis for many affected individuals remains unknown. Here, we identified a deleterious hemizygous variant of X-linked retinoblastoma-binding protein 7 (RBBP7) as a potential key cause of MA, which was also found to be associated with the development of Leydig cell tumors. This mutation resulted in premature protein translation termination, affecting the sixth WD40 domain of the RBBP7 and the interaction of the mutated RBBP7 with histone H4. Decreased BRCA1 and increased γH2AX were observed in the proband. In mouse spermatogonial and pachytene spermatocyte-derived cells, deprivation of rbbp7 led to cell cycle arrest and apoptosis. In Drosophila, knockdown of RBBP7/Caf1-55 in germ cells resulted in complete absence of germ cells and reduced testis size, whereas knockdown of RBBP7/Caf1-55 in cyst cells resulted in hyperproliferative testicular cells. Interestingly, male infertility caused by Caf1-55 deficiency was rescued by ectopic expression of wild-type human RBBP7 but not mutant variants, suggesting the importance of RBBP7 in spermatogenesis. Our study provides insights into the mechanisms underlying the co-occurrence of MA and testicular tumors and may pave the way for innovative genetic diagnostics of these 2 diseases.

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RBBP7

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