| 2018 |
PCGF5 is required for neural differentiation of mouse embryonic stem cells (mESCs); loss of PCGF5 blocks neural differentiation by activating the SMAD2/TGF-β signaling pathway and impairs reduction of H2AK119ub1 and H3K27me3 around neural-specific genes, keeping them repressed. |
CRISPR/Cas9 knockout in mESCs, RNA-seq, ChIP-seq, rescue experiments |
Nature communications |
High |
29765032
|
| 2017 |
PCGF3 and PCGF5 function as transcriptional activators in ES cells through interaction with the pluripotency factor Tex10 and the co-activator p300; Pcgf3/5 deletion reduces Tex10 and p300 occupancy at target genes and globally reduces H2AK119ub1 levels; Pcgf3/5 are required for mesoderm differentiation. |
CRISPR/Cas9 knockout, RNA-seq, proteomic interactome (MS), ChIP/promoter occupancy analysis, in vitro and in vivo differentiation assays |
The Journal of biological chemistry |
High |
29054931
|
| 2016 |
Pcgf5 deletion in hematopoietic stem and progenitor cells (HSPCs) causes significant reduction in global H2AK119ub1 levels but does not impair HSPC self-renewal or repopulating capacity, indicating that Pcgf5-containing PRC1 functions as a histone modifier in vivo but its role in HSPCs is compensated by other PRC1-related complexes. |
Conditional Cre-ERT knockout in mice, competitive bone marrow transplantation, ChIP-seq for H2AK119ub1, flow cytometry |
PloS one |
High |
27136092
|
| 2018 |
During E. chaffeensis infection, the bacterial effector TRP120 interacts with PCGF5 (and other PCGF isoforms) in the nucleus early in infection; PCGF isoforms are redistributed from the nucleus to the ehrlichial vacuole and subsequently undergo proteasomal degradation; this disrupts PRC1-mediated H2AK119ub1 repressive marks and alters HOXB/HOXC gene transcription; siRNA knockdown of PCGF isoforms increases E. chaffeensis infection. |
Ectopic expression and co-immunoprecipitation of TRP120, confocal immunofluorescence microscopy, siRNA knockdown, proteasome inhibitor treatment, ChIP for H2AK119ub1 |
Infection and immunity |
High |
29358333
|
| 2017 |
The E. chaffeensis effector TRP120 acts as a HECT E3 ubiquitin ligase that polyubiquitinates PCGF5, leading to reduced PCGF5 protein levels; this activity depends on Nedd4L, which also mediates TRP120 ubiquitination; Nedd4L knockdown reduces TRP120-Ub, decreases ehrlichial infection, and reduces PCGF5 recruitment to ehrlichial inclusions. |
In vitro ubiquitination assay with purified TRP120 and E2 enzymes, ectopic expression of HECT catalytic-site mutant, Nedd4L siRNA knockdown, immunoprecipitation |
Infection and immunity |
High |
28630068
|
| 2018 |
During blood specification, SCL/TAL1 directly activates expression of PCGF5 (along with RYBP) as part of a Polycomb-PRC1 co-repressor program that suppresses alternative cardiac/paraxial lineage gene expression; PCGF5 and RYBP co-occupy SCL target genes including cardiac/paraxial loci; reduction of Rybp expression mimics the Scl-null cardiac phenotype. |
Scl-null mouse model, RNA-seq, ChIP-seq for RYBP and H2AK119ub1/H3K27me3, genome-wide ChIP, genetic rescue (Eto2/Rybp knockdown) |
Nature communications |
Medium |
30560907
|
| 2018 |
A variant PRC1 complex incorporating PCGF3 and PCGF5 represses Meis2 expression in the distal mouse forelimb bud; PcG factors and retinoic acid-related signals antagonize each other to polarize Meis2 expression along the proximal-distal axis. |
Mouse genetic models, mathematical modeling, in vivo gene expression analysis |
Development (Cambridge, England) |
Medium |
30190278
|
| 2009 |
The E. chaffeensis TRP47 effector interacts with PCGF5; the amino-terminal truncated form of p47 containing tandem repeats interacts with PCGF5 but not with FYN, PTPN2, or CAP1, establishing that the TR domain of p47 is sufficient for PCGF5 interaction; interaction confirmed by co-immunoprecipitation and colocalization in HeLa cells. |
Yeast two-hybrid, co-immunoprecipitation, colocalization by confocal fluorescence microscopy in HeLa cells transfected with AcGFP1-p47 |
Infection and immunity |
Medium |
19273555
|
| 2011 |
The E. chaffeensis TRP120 effector interacts with PCGF5; the TR domain of TRP120 is sufficient for interaction with PCGF5 specifically, while other host targets require additional TRP120 domains; TRP120 and PCGF5 strongly colocalize in HeLa cells and near ehrlichial morulae. |
Yeast two-hybrid cotransformation confirmation, colocalization by fluorescence microscopy in HeLa cells |
Infection and immunity |
Medium |
21859857
|
| 2019 |
PCGF5 interacts exclusively with the long isoform of AUTS2 (not the short isoform), as identified by yeast two-hybrid screen; PCGF3 expression levels influence the ability of the long AUTS2 isoform to activate or repress transcription, placing PCGF5 in the long-isoform-specific AUTS2-PRC1 complex. |
Yeast two-hybrid screen, reporter transcriptional assays |
Molecular psychiatry |
Low |
30953002
|
| 2014 |
SUMO pathway inhibition significantly reduced recruitment of PCGF5 to E. chaffeensis ehrlichial inclusions (TRP120-interacting protein), demonstrating that SUMO-dependent interactions are required for PCGF5 localization to the bacterial inclusion during infection. |
Small-molecule SUMO pathway inhibitor treatment, confocal colocalization microscopy, co-immunoprecipitation |
Infection and immunity |
Medium |
25047847
|
| 2016 |
In T-ALL cells, PCGF5 represses transcription of the NKL homeobox gene MSX1, while AUTS2 (as part of PRC1.5/PRC1 subtype 5) activates it; expression profiling and functional analyses demonstrate opposing activities of PCGF5 and AUTS2 on MSX1 transcription. |
Expression profiling, forced-expression experiments, pharmacological EZH2 inhibition, H3K27me3 ChIP analysis in T-ALL cell lines |
Oncotarget |
Medium |
27322685
|
| 2024 |
Pcgf5 suppresses Wnt3 expression via activation of the Notch1/Hes1 signaling axis, thereby governing the differentiation fate of neural stem cells; knockdown of Pcgf5 in P19 cells decreases neuronal markers (Sox2, Zfp521, Pax6) while increasing pluripotency markers (Oct4, Nanog), and knockdown of pcgf5a by morpholino in zebrafish causes neurodevelopmental defects. |
siRNA knockdown and overexpression in P19 cells, zebrafish morpholino knockdown, qRT-PCR, in vivo neural marker analysis |
Heliyon |
Medium |
38533065
|
| 2020 |
Pcgf5 knockout in mESCs delays generation of the three germ layers (especially ectoderm), impairs epithelial-mesenchymal transition during embryoid body morphogenesis, differentially affects Nodal and Wnt signaling gene expression, and induces repression of Notch pathway genes leading to enhanced cardiomyocyte maturation and dampened ectodermal-neural differentiation. |
CRISPR/Cas9 KO mESCs, embryoid body differentiation protocol, gene expression analysis |
Development, growth & differentiation |
Medium |
32130724
|
| 2025 |
Pcgf5 forms a chimeric transcript with MT2C_Mm (MERVL long terminal repeat) during zygotic genome activation (ZGA); Pcgf5 knockdown reduces H3K27me3 and H2AK119ub1 in mouse preimplantation embryos, upregulates ZGA genes and imprinting genes, and impairs H3K27me3 addition to the maternal Xist region, implicating Pcgf5 in noncanonical imprinting and Xist regulation. |
Morpholino knockdown in mouse embryos, ChIP for H3K27me3 and H2AK119ub1, developmental rate tracking, gene expression analysis |
bioRxivpreprint |
Medium |
bio_10.1101_2025.01.24.632300
|
| 2023 |
PCGF5 is among a minority of Xist-recruited proteins that form Xist-seeded protein assemblies at the inactive X chromosome, placing it in the supramolecular assembly that drives X-chromosome inactivation. |
Protein assembly and localization analysis at the inactive X chromosome (described in the context of CIZ1-focused study) |
Frontiers in cell and developmental biology |
Low |
38155839
|
| 2025 |
WDR68/DCAF7 interacts with PCGF5 (and AUTS2) as identified by co-immunoprecipitation coupled with LC-MS, placing PCGF5 in the WDR68 interactome relevant to mouse embryonic development. |
Co-immunoprecipitation combined with liquid chromatography-mass spectrometry (Co-IP/LC-MS) |
Journal of translational medicine |
Low |
40462101
|