PCGF3 antibody - middle region (ARP34416_P050)
- Known as:
- PCGF3 (anti-) - middle region (ARP34416_P050)
- Catalog number:
- arp34416_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PCGF3 antibody - middle region (ARP34416_P050)
Related genes to: PCGF3 antibody - middle region (ARP34416_P050)
- Gene:
- PCGF3 NIH gene
- Name:
- polycomb group ring finger 3
- Previous symbol:
- RNF3
- Synonyms:
- FLJ36550, DONG1, RNF3A, MGC40413
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2014-11-19
Related products to: PCGF3 antibody - middle region (ARP34416_P050)
Related articles to: PCGF3 antibody - middle region (ARP34416_P050)
- [This corrects the article DOI: 10.3389/fcimb.2024.1421195.]. - Source: PubMed
Publication date: 2026/03/06
Chen JingYin QiXu ShihengTan XiaoqingLiang YuChen ChaohuiLi LiZhang TaoShen Tao - Polycomb group proteins mediate epigenetic repression via multisubunit complexes, including canonical Polycomb Repressive Complex 1 (PRC1), which monoubiquitylates histone H2A and binds histone H3 trimethylated at lysine-27 (H3K27me3). The RING1 subunit of PRC1, critical for H2A ubiquitylation, forms other complexes. These variant RING1 complexes also ubiquitylate H2A but cannot bind H3K27me3, and their role in epigenetic repression is debated. Using genetics, we found that canonical PRC1 and variant RING1 complexes ubiquitylate H2A at distinct genomic regions. We established that the PCGF protein specific for variant RING1 complexes, which we named Siesta, is not required for epigenetic repression of developmental genes but controls larval locomotion independently of H2A ubiquitylation. Leveraging a massively parallel transgenic approach, we demonstrated that H2A ubiquitylation has minimal impact on transcriptional repression. Our findings imply that Siesta-RING1 complexes operate outside the Polycomb regulatory system and that the popular PRC1 classification will benefit from revision. - Source: PubMed
Publication date: 2026/03/06
Kahn Tatyana GGarrido AndresYushkova AnastasiyaKim MariaGlotov AlexanderSreekumar SwedaLarsson JanSchwartz Yuri B - Type I interferons （IFN-I） are key proteins in antiviral response and immunomodulation. Negative regulators avoid abnormal activation of the interferon pathway or overactivation of interferon-activating proteins through multiple mechanisms. Loss-of-function mutations in negative regulator genes lead to the development of a variety of type I interferonopathy. It is of great significance in theory and clinic to discover new negative regulators and study their functions, but there is no effective screening system at present. Here, a screening system is established through a resistance reporter, which is designed to be expressed only in cells with interferon pathway activation. In conjunction with CRISPR knockout library, cells are screened for interferon pathway activation due to knockout of negatively regulators, which led to the identification of negatively regulator candidate genes such as PCGF3/5, UCK2, and ITPKA. The expression products of these genes functioned by targeting MAVS and promoted EMCV (encephalomyocarditis virus) infection by inhibiting interferon pathway activation. This study deepens the understanding of the regulatory network of the interferon pathway and provides a new theoretical basis for the study of the pathogenesis of autoimmune diseases. - Source: PubMed
Publication date: 2025/08/19
Pang ZhaojunYang HanLi BoLiu YifuZhao ZhenxiangZhu ZixiangPeng ShouchunMu XinYu Hongjian - DNA methylation in brain regions represents a potential mechanism linking genetic variation to Alzheimer's disease (ad) risk, yet most studies have focused on blood-derived methylation markers. In this study, we conducted a systematic Mendelian randomization (MR) study to evaluate associations between predicted brain region-specific DNA methylation levels and ad risk, using methylation quantitative trait loci (mQTL) as genetic instruments. - Source: PubMed
Zhong HuaZhu JingjingLiu ShuaiZhou DanLong QuanWu ChongZhao BingxinCheng ChaoYang YaohuaWu QingWu YongLi ChangweiWang ZhaomingWu JianyongGuo XingyiZhi DeguiDeng YoupingWu Lang - Neocortex development is characterized by sequential phases of neural progenitor cell (NPC) expansion, neurogenesis, and gliogenesis. Polycomb-mediated epigenetic mechanisms are known to play important roles in regulating the lineage potential of NPCs during development. The composition of Polycomb repressive complex 1 (PRC1) is highly diverse in mammals and was hypothesized to contribute to context-specific regulation of cell fate. Here, we have performed a side-by-side comparison of the role of canonical PRC1.2/1.4 and non-canonical PRC1.3/1.5, all of which are expressed in the developing neocortex, in NSC proliferation and differentiation. We found that the deletion of in NSCs led to a strong reduction in proliferation and to altered lineage fate, both during the neurogenic and gliogenic phase, whereas played a minor role. Mechanistically, genes encoding stem cell and neurogenic factors were bound by PRC1 and differentially expressed upon deletion. Thus, rather than different PRC1 subcomplexes contributing to different phases of neural development, we found that canonical PRC1 played a more significant role in NSC regulation during proliferative, neurogenic, and gliogenic phases compared with non-canonical PRC1. - Source: PubMed
Publication date: 2025/02/11
Hoffmann JanineSchütze Theresa MKolodziejczyk AnnikaKüster KarolinKränkel AnnekathrinReinhardt SusanneDerihaci Razvan PBirdir CahitWimberger PaulineKoseki HaruhikoAlbert Mareike