Ask about this productRelated genes to: PCGF1 antibody
- Gene:
- PCGF1 NIH gene
- Name:
- polycomb group ring finger 1
- Previous symbol:
- -
- Synonyms:
- NSPC1, RNF68, MGC10882
- Chromosome:
- 2p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-17
- Date modifiied:
- 2014-11-19
Related products to: PCGF1 antibody
Related articles to: PCGF1 antibody
- Germinal center (GC) B cell-like diffuse large B cell lymphoma (GCB-DLBCL) depends on the cooperative activity of the histone methyltransferases DOT1L and EZH2 to maintain its pro-proliferative GCB cell identity while repressing plasma cell (PC) differentiation. To explore the mechanisms underlying the co-dependency between DOT1L and EZH2 in GCB-DLBCL, we performed an EZH2 inhibition (EZH2i)-anchored genome-wide CRISPR interference screen and identified multiple candidate genes encoding components of non-canonical (nc) PRC1 complexes, including USP7, KDM2B, RING1, and PCGF1. We identified USP7 as potential direct target of DOT1L, whose downregulation was associated with increased EZH2i sensitivity in multiple GCB-DLBCL cell lines. Furthermore, we observed that DOT1L influences the composition of chromatin-bound ncPRC1 complexes and regulates, in part, the deposition of H2AK119 monoubiquitination (H2AK119ub1) at gene promoters co-occupied by H3K27me3, here defined as PRC1/2 targets. These PRC1/2 targets were specifically enriched in PC signature genes, whose derepression was associated with DOT1L inhibition (DOT1Li)-mediated loss of H2AK119ub1. This study reveals novel insights into the role of DOT1L and its functional co-dependence with EZH2 in maintaining GCB identity in DLBCL, supporting a model in which concurrent reduction of H2AK119ub1 and H3K27me3 promotes differentiation toward an anti-proliferative, plasma cell-like state. - Source: PubMed
Publication date: 2026/05/29
Göbel CamielNiccolai RacheleGregoricchio Sebastiande Groot Marnix Hugo PhilipKneefel Stijn F KKreft MaaikeKuiken Hendrik JLieftink CorEickhoff NilsHoekman LiesbethBleijerveld OnnoZwart WilbertBeijersbergen Roderick Lvan Leeuwen FredJacobs Heinz - Inadequate antigen presentation, driven by epigenetic repression of major histocompatibility complex class I (MHC-I), represents a fundamental barrier to effective cancer immunotherapy. Here, we identify polycomb group ring finger 1 (PCGF1) as a tumor cell-intrinsic epigenetic repressor of MHC-I through a genome-wide CRISPR screen. Genetic ablation of PCGF1 alone is sufficient to relieve repressive histone modifications (H2AK119ub and H3K27me3) at both the MHC-I gene cluster and its master regulator NLRC5, thereby restoring cell-surface antigen presentation and immunotherapy sensitivity. Building on this epigenetic foundation, we introduce modular engineering strategies to enhance translational robustness against tumor antigen heterogeneity. Specifically, CRISPR activation (CRISPRa) is used to broaden the repertoire of endogenous tumor antigens without altering the restored antigen presentation machinery. These epigenetically reprogrammed cells are subsequently cryoinactivated and formulated into an injectable thermosensitive chitosan-based hydrogel, in which manganese-mediated STING activation serves as an immunostimulatory adjuvant to amplify antigen capture and systemic T-cell priming.Collectively, this study establishes epigenetic reprogramming of antigen presentation as a foundational principle for whole-cell vaccine design and demonstrates how modular antigen and innate immune augmentation can enhance therapeutic robustness without obscuring the core mechanism. This platform offers a rational and adaptable framework for overcoming immune resistance in next-generation cancer immunotherapy. - Source: PubMed
Publication date: 2026/03/28
Li XiaodiZong XiaoqingYuan PengfeiYan XiaodieYang CaiqiChen XinjieWei SiyingWen YaoqiDu JingruLiu XiangLiu FengyingDai Jian - KMT2A-rearranged acute myeloid leukemia is driven by epigenetic dependencies yet remains clinically resistant to therapies targeting individual regulators, indicating that resistance reflects compensatory regulation across an epigenetic network. A systematic understanding of this compensatory network has been lacking. To address this gap, we utilized Perturb-seq screening to systematically map the functional architecture of this network. We uncovered a compensatory epigenetic circuit, where a synergistic hub including KAT6A, Menin, and DOT1L converges to silence a core differentiation program (the 'Myeloid Program'), thereby maintaining leukemic identity. The activity of this program strongly correlated with favorable survival in large patient cohorts. While individual perturbations of hub components only partially derepress this program, their simultaneous pharmacological inhibition collapses the circuit's buffering capacity, leading to robust reactivation of the Myeloid Program and potent synergistic anti-leukemic activity. Our model also shows that disruption of antagonistic regulators of the Myeloid Program, such as the PRC1.1 component PCGF1, confers strong resistance to DOT1L inhibition. Finally, the Myeloid Program is a predictive biomarker, where high baseline activity defined a vulnerable state that could be selectively targeted by MEK, AKT, and mTOR inhibitors. Together, these findings establish a framework for identifying circuit-level epigenetic compensation and for rationally designing precision combination therapies that restore differentiation or target state-dependent vulnerabilities in acute myeloid leukemia. - Source: PubMed
Publication date: 2026/03/25
Aryal SajesanCurtiss Brittany MZhou XinyueLu RuiCheng Changde - - Source: PubMed
Publication date: 2026/02/11
Chen PanYang XuejieChen RuhaiLi HanluMa JingwenChang JingHong GuangliangLiu WeiQuan XiongzhiYin BinHou LinQiang BoqinShu PengchengHe JiangpingPeng XiaozhongChen Jiekai - Allergic asthma pathogenesis encompasses systemic immune, metabolic, and epithelial barrier dysfunction; however, minimally invasive tools to longitudinally explore these processes remain limited. - Source: PubMed
Publication date: 2026/01/06
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