Ask about this productRelated genes to: CHAF1B antibody
- Gene:
- CHAF1B NIH gene
- Name:
- chromatin assembly factor 1 subunit B
- Previous symbol:
- -
- Synonyms:
- CAF1P60, CAF-1, CAF1, CAF1A, MPP7, MPHOSPH7
- Chromosome:
- 21q22.12-q22.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-29
- Date modifiied:
- 2018-02-13
Related products to: CHAF1B antibody
Related articles to: CHAF1B antibody
- BCL6 is a master regulator of germinal center (GC) B cells. Further identification and characterization of factors that may play a role within the BCL6 network is important for our understanding of GC B cell differentiation and function. Here, through co-Immunoprecipitation coupled with mass spectrometry, we identify CHAF1B as a new partner in the BCL6 complex, which is highly expressed in GC B cells, promoting GC formation and humoral immunity. Loss of CHAF1B impairs the dark zone (DZ) and light zone (LZ) organization and induces apoptosis, resulting in abnormal GC responses and antibody production. Mechanistically, CHAF1B stabilizes BCL6/TBL1XR1 complex to promote GC B cell differentiation by cooperative transcriptional repression. Furthermore, overexpression of CHAF1B in B cells reduces the plasmablast by extending GC reaction, which is positively related to the production of high affinity antibodies in response to vaccines or pathogens. These findings not only advance the understanding of GC biology but also had potential implications for developing targeted strategies to improve vaccination efficacy. - Source: PubMed
Chen AchunYuan QuyuLi DaiyingYuan JiayiLin YingtongMa XiancaiZhang XuChen YanDong JunchaoZhou NanZhang HuiPan TingZhang XueHe Xin - The clinical relevance of non-HLA antibodies remains uncertain due to the lack of standardized assays. This study aimed to assess comparative reference values for non-HLA antibody profiles in a cohort of kidney transplant candidates on the deceased donor waiting list (WL group) with 0% calculated panel reactive antibodies (cPRA) and in healthy male blood donors (BD group). - Source: PubMed
Publication date: 2026/02/13
Quintiliano AAgrawal AZuccarelli MWakefield L LSchinstock C AGandhi M JBentall A J - Glioblastoma (GBM), the most aggressive tumor in the adult central nervous system, remains a major therapeutic challenge due to its high recurrence and resistance to conventional therapies. Recent evidence underscores the pivotal role of glioma stem cells (GSCs) in driving these malignant features. In this study, using intracranial xenograft models established in 4-week-old male BALB/c nude mice and patient-derived primary GSCs, we uncover a critical function of the chromatin assembly factor subunit Chaf1b in sustaining the stemness of GSCs and modulating the tumor immune microenvironment. We show that Chaf1b is markedly overexpressed in high-grade gliomas and GSC populations. Genetic silencing of Chaf1b led to a significant reduction in GSC self-renewal capacity and tumorigenicity, both in vitro and in intracranial xenograft models. Mechanistically, Chaf1b was found to upregulate IL-33 secretion, thereby promoting microglial M2 polarization and activating the PI3K/AKT signaling pathway-effects that were reversible upon IL-33 neutralization. These findings position Chaf1b as a key mediator of GBM aggressiveness and suggest it as a promising target for disrupting the stem-immune axis in GBM. - Source: PubMed
Publication date: 2025/12/03
He Yong-LinNiu LiangWang ChenLiao Zhi-PengLiu KaiGao ShuoDu Ai-ChaoLiu Wei-GuoJia JuanZhang Yu-BoYin HangYuan Guo-QiangPan Ya-Wen - Chromatin assembly factor 1B (CHAF1B), a pivotal regulator of chromatin assembly following DNA replication, has been implicated in oncogenic processes. However, its role in sorafenib resistance and potential anti-tumor mechanisms in hepatocellular carcinoma (HCC) remain unclear. This study has sought to elucidate CHAF1B's therapeutic potential and its potential synergistic role with sorafenib in overcoming chemoresistance. In this study, bioinformatics, immunohistochemistry, western blot, CCK8, colony formation, transwell migration and invasion, and flow cytometry were performed to analyze the correlation between CHAF1B and sorafenib resistance in HCC. Furthermore, RNA sequencing (RNA-seq), combined with signaling pathway-specific inhibitors, was used to elucidate the specific role of CHAF1B in sorafenib resistance of HCC and its related mechanism. CHAF1B was significantly upregulated in HCC tissues and sorafenib-resistant HCC cells, with elevated expression correlated with reduced survival probability in HCC patients. Moreover, high CHAF1B levels predicted poorer clinical outcomes in sorafenib-treated patients. Functional assays revealed that CHAF1B promotes HCC cell proliferation, migration, and invasion, while also enhancing resistance to sorafenib. In contrast, knockdown of CHAF1B significantly increased sorafenib-induced inhibition of proliferation and cell death. Mechanistically, CHAF1B facilitated malignant phenotypes via activation of the PI3K/Akt/HIF-1α pathway. Furthermore, blockade of PI3K/Akt/HIF-1α signaling partially attenuated the CHAF1B-mediated sorafenib resistance. CHAF1B is a key regulator of sorafenib resistance, and targeting CHAF1B in conjunction with sorafenib may represent a promising therapeutic approach for HCC by modulating the PI3K/Akt/HIF-1α signaling axis. - Source: PubMed
Publication date: 2025/09/22
Zhuo WenfengZhao JialiZheng ZhouyingCai ShanglinZeng GuifangLin EnBai ZiruiWang BoJia YingbinLi PeipingLi Jian - Immunoglobulin A nephropathy (IgAN) stands as the most prevalent primary glomerulonephritis globally, almost half of patients progress to end-stage kidney disease (ESKD). However, the precise pathogenesis of IgAN remains elusive. Long non-coding RNAs (lncRNAs), non-protein-coding transcripts that regulate gene expression, have been found to exhibit distinct expression patterns in various disease states. Comprehensive bioinformatic analyses from IgAN patients have uncovered differential expression of lncRNAs such as , , and . Furthermore, a single nucleotide polymorphism in has been linked to IgAN susceptibility and correlated with clinical markers like urinary red blood cells and hemoglobin levels. and , specifically expressed in the kidneys of IgAN patients, exhibit associations with renal fibrosis indices and the degree of kidney function deterioration, influencing the progression of renal fibrosis through distinct signaling pathways. Additionally, renal intercellular adhesion molecule 1 (ICAM-1) related long noncoding RNA () levels positively correlate with IgAN severity and contribute to renal fibrosis, whereas serum serves as an independent protective factor against IgAN. Notably, experiments have validated the involvement of , , and in the pathogenesis of IgAN. Nevertheless, data on the roles of lncRNAs in IgAN pathogenesis and their potential as biomarkers remain limited, and effective therapeutic options for IgAN are similarly rare. Therefore, there is an urgent need to bridge this knowledge gap. This article presents a review of current literature on lncRNAs related to IgAN, aiming to consolidate existing findings and identify future research avenues. - Source: PubMed
Publication date: 2025/05/06
Huang XiaoxuanChen LanHe JinxuanTang JianhuiMou Zhixiang