PCGF3

Last update 08 May 2025

Basic Info

Synonyms

DONG1, FLJ36550, MGC40413

+ [6]

Introduction

Component of a Polycomb group (PcG) multiprotein PRC1-like complex, a complex class required to maintain the transcriptionally repressive state of many genes, including Hox genes, throughout development. PcG PRC1 complex acts via chromatin remodeling and modification of histones; it mediates monoubiquitination of histone H2A 'Lys-119', rendering chromatin heritably changed in its expressibility. Within the PRC1-like complex, regulates RNF2 ubiquitin ligase activity (PubMed:26151332). Plays a redundant role with PCGF5 as part of a PRC1-like complex that mediates monoubiquitination of histone H2A 'Lys-119' on the X chromosome and is required for normal silencing of one copy of the X chromosome in XX females (By similarity).

100 Clinical Results associated with PCGF3

100 Translational Medicine associated with PCGF3

0 Patents (Medical) associated with PCGF3

Literatures (Medical) associated with PCGF3

01 Jul 2024·Applied Biochemistry and Biotechnology

ceRNA Network Analysis Reveals Potential Key miRNAs and Target Genes in COVID-19-Related Chronic Obstructive Pulmonary Disease

Article

Author: Jia, Xiaodong ; Yu, Tong ; Zhang, Lihai ; Geng, Zhangyan ; Zhang, Zhipeng ; Yuan, Lindong

The continued spread of SARS-CoV-2 has presented unprecedented obstacles to the worldwide public health system. Especially, individuals with chronic obstructive pulmonary disease (COPD) are at a heightened risk of contracting SARS-CoV-2 infection due to their pre-existing respiratory symptoms that are not well-managed. However, the viral mechanism of affecting the expression of host genes, COPD progression, and prognosis is not clear yet.This study integrated the differential expression information of COPD patients and then calculated the correlation between mRNAs and miRNAs to construct a COPD-specific ceRNA network. The DEGs of individuals with SARS-CoV-2 infection and anticipated miRNAs and their targets were analyzed in 9 SARS-CoV-2 sequences from different geographic locations. Furthermore, combining the experimentally validated miRNAs and genes, the regulatory miRNA-mRNA relationships were identified. All the regulatory relationships were integrated into the COPD-specific network and the network modules were explored to get insight into the functional mechanism of SARS-CoV-2 infection in COPD patients.A higher proportion of DEGs compete with the same miRNA suggesting a higher expression of genes in the COPD-specific ceRNA network. Hsa-miR-21-3p is the largest connected point in the network, but the proportion of genes upregulated by hsa-miR-21-3p is low (P = 0.1406). This indicates that the regulatory relationship of competitive inhibition has little effect on has-miR-21, and the high expression pattern is a poor prognostic factor in COPD. Hsa-miR-15a-5p is the most significant miRNA with the highest proportion of DEGs. And ANXA2P3 is the only gene in the COPD ceRNA network that interferes with hsa-miR-15a-5p. In addition, we found that has-miR-1184- and has-miR-99-cored modules were significant, and genes ZDHHC18, PCGF3, and KIAA0319L interacting with them were all associated with COPD prognosis, and high expression of these genes could lead to poor prognosis in COPD.The key regulators such as miR-21, miR-15a, ANXA2P3, ZDHHC18, PCGF3, and KIAA0319L can be used as prognostic biomarkers for early intervention in COPD with SARS-CoV-2 infection.

01 May 2023·Genes, Chromosomes and Cancer

Non‐synonymous, synonymous, and non‐coding nucleotide variants contribute to recurrently altered biological processes during retinoblastoma progression

Article

Author: Berry, Jesse L. ; Stachelek, Kevin ; Kim, Jonathan ; Lee, Thomas C. ; Murphree, A. Linn ; Xu, Liya ; Harutyunyan, Narine ; Aparicio, Jennifer G. ; Cobrinik, David ; Nagiel, Aaron ; Beck, Assaf ; Reynolds, C. Patrick ; Lee, Susan

AbstractRetinoblastomas form in response to biallelic RB1 mutations or MYCN amplification and progress to more aggressive and therapy‐resistant phenotypes through accumulation of secondary genomic changes. Progression‐related changes include recurrent somatic copy number alterations and typically non‐recurrent nucleotide variants, including synonymous and non‐coding variants, whose significance has been unclear. To determine if nucleotide variants recurrently affect specific biological processes, we identified altered genes and over‐represented variant gene ontologies in 168 exome or whole‐genome‐sequenced retinoblastomas and 12 tumor‐matched cell lines. In addition to RB1 mutations, MYCN amplification, and established retinoblastoma somatic copy number alterations, the analyses revealed enrichment of variant genes related to diverse biological processes including histone monoubiquitination, mRNA processing (P) body assembly, and mitotic sister chromatid segregation and cytokinesis. Importantly, non‐coding and synonymous variants increased the enrichment significance of each over‐represented biological process term. To assess the effects of such mutations, we examined the consequences of a 3′ UTR variant of PCGF3 (a BCOR‐binding component of Polycomb repressive complex I), dual 3′ UTR variants of CDC14B (a regulator of sister chromatid segregation), and a synonymous variant of DYNC1H1 (a regulator of P‐body assembly). One PCGF3 and one of two CDC14B 3′ UTR variants impaired gene expression whereas a base‐edited DYNC1H1 synonymous variant altered protease sensitivity and stability. Retinoblastoma cell lines retained only ~50% of variants detected in tumors and enriched for new variants affecting p53 signaling. These findings reveal potentially important differences in retinoblastoma cell lines and tumors and implicate synonymous and non‐coding variants, along with non‐synonymous variants, in retinoblastoma oncogenesis.

01 Jun 2022·Molecular Genetics & Genomic MedicineQ4 · MEDICINE

Imputed expression of schizophrenia‐associated genes and cognitive measures in patients with schizophrenia

Q4 · MEDICINE

ArticleOA

Author: Fabbri, Chiara ; Drago, Filippo ; Serretti, Alessandro ; Leggio, Gian Marco

AbstractBackgroundCognitive dysfunction is a core manifestation of schizophrenia and one of the best predictors of long‐term disability. Genes increasing risk for schizophrenia may partly act through the modulation of cognition.MethodsWe imputed the expression of 130 genes recently prioritized for association with schizophrenia, using PsychENCODE variant weights and genotypes of patients with schizophrenia in CATIE. Processing speed, reasoning, verbal memory, working memory, vigilance, and a composite cognitive score were used as phenotypes. We performed linear regression models for each cognitive measure and gene expression score, adjusting for age, years of education, antipsychotic treatment, years since the first antipsychotic treatment and population principal components.ResultsWe included 425 patients and expression scores of 91 genes (others had no heritable expression; Bonferroni corrected alpha = 5.49e‐4). No gene expression score was associated with cognitive measures, though ENOX1 expression was very close to the threshold for verbal memory (p = 6e‐4) and processing speed (p = 7e‐4). Other genes were nominally associated with multiple phenotypes (MAN2A1 and PCGF3).ConclusionA better understanding of the mechanisms mediating cognitive dysfunction in schizophrenia may help in the definition of disease prognosis and in the identification of new treatments, as the treatment of cognitive impairment remains an unmet therapeutic need.

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