Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Multi-omics integration identifies progenitor-state specific PBRM1-PIAS1 cooperation in repressing differentiation in epithelial tissue

ABSTRACT: Here we determine the gene targets controlled by PBRM1-PIAS1 cooperation in regulating epidermal differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE228221 | GEO | 2024/01/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Multi-omics integration identifies progenitor-state specific PBRM1-PIAS1 cooperation in repressing differentiation in epithelial tissue

Project description:Multi-omics integration identifies progenitor-state specific PBRM1-PIAS1 cooperation in repressing differentiation in epithelial tissue

| PRJNA948849 | ENA

Effect of PIAS1 on gene expression

2014-02-06 | GSE44024 | GEO

Effect of PIAS1 on gene expression

Project description:To study the effect of PIAS1 on transcriptional regulation, we establishedstable PIAS1 shRNA knockdown cells in breast cancer cell line MDA-MB231. By comparing the expression profiles of control vs PIAS1 knockdown cells, we can identify potential PIAS1 target genes involved in breast tumorigenesis. MDA-MB231 Control shRNA and PIAS1 shRNA2 cells were cultured in DMEM plus 10% FBS (DMEM) or SCM for 30 h, and total RNA was used for microarray.

2014-02-06 | E-GEOD-44024 | biostudies-arrayexpress

PBRM1 Knockdown in RCC Cell Lines

Project description:PBRM1 was found to be mutated in a high percentage of clear cell RCCs. We performed knockdown of PBRM1 via siRNA and compared with scrambled control in three different RCC cell lines. PBRM1 siRNA and mock treated cell lines were normalized together with 'hypoxic' clear cell renal tumors and normal renal tissue samples from GSE17818.

2011-01-20 | E-GEOD-22316 | biostudies-arrayexpress

PIAS1 is a target gene selective androgen receptor coregulator in prostate cancer cell chromatin

Project description:To study the importance of PIAS1 (protein inhibitor of activated STAT1) for the androgen-regulated transcriptome of VCaP prostate cancer cells, we silenced its expression by RNAi. Transcriptome analyses revealed that a subset of the androgen-regulated genes is significantly influenced, either activated or repressed, by PIAS1 depletion. The depletion also exposed a completely new set of genes to androgen regulation, suggesting that PIAS1 can mask genes from androgen receptor (AR). Pathway analyses of gene expression data suggest involvement of PIAS1 in VCaP cell proliferation. According to genome-wide ChIP-seq analyses, PIAS1 interacts with the AR on chromatin harboring also SUMO2/3, as androgen exposure multiplied the occupancy of PIAS1 in the chromatin, and resulted in nearly complete overlap with AR chromatin binding events. PIAS1 interacted also with pioneer factor FOXA1 in the chromatin. Our results strongly suggest that PIAS1 is a genuine chromatin-bound coregulator of AR which functions in a target gene selective fashion in prostate cancer cells.

2015-01-02 | GSE56086 | GEO

PBRM1 deficiency is synthetic lethal with PARP inhibitors in human cancers

Project description:Polybromo-1 (PBRM1), which encodes a specific subunit of the pBAF chromatin remodeling complex, is inactivated in multiple malignancies including 50% of clear cell renal cell carcinoma. At present, a therapeutic strategy that selectively targets PBRM1 defects does not exist. PBRM1 is involved in multiple cellular processes including transcription, replication and DNA repair. Using high-throughput screens and multiple isogenic and non-isogenic models, we found that PBRM1 defects cause synthetic lethality with several clinical PARP inhibitors, both in vitro and in vivo. This effect was enhanced using combinations with either small molecule ATR or BET inhibitors. Mechanistically, PBRM1 defects caused increased replication stress, R-loop formation and genomic instability that was exacerbated by PARP inhibitors. We also found that PARP and ATR inhibitors activate the cGAS-STING innate immunity pathway in PBRM1-deficient but not in PBRM1-proficient cells. These data provide the pre-clinical rationale for assessing PARP inhibitors as a monotherapy or in combination with ATR inhibitors or immune checkpoint inhibitors, in patients with PBRM1-deficient cancers.

2022-02-21 | PXD017826 | Pride

Quantitative proteomics identifies novel PIAS1 protein substrates involved in cell migration and motility

Project description:The Protein Inhibitor of Activated STAT 1 (PIAS1) is an E3 SUMO ligase that plays important roles in various cellular pathways, including STAT signaling, p53 pathway, and the steroid hormone signaling pathway. PIAS1 can SUMOylate PML (at Lys-65 and Lys-160) and PML-RARα promoting their ubiquitin-mediated degradation. Increasing evidence shows that PIAS1 is overexpressed in various human malignancies, such as prostate and lung cancers. To understand the mechanism of action of PIAS1, we developed a quantitative SUMO proteomic approach to identify potential substrates of PIAS1 in a system-wide manner. Our analyses enabled the profiling of 983 SUMO sites on 544 proteins, of which 204 SUMO sites on 123 proteins were identified as putative PIAS1 substrates. These substrates were found to be involved in different cellular processes, including transcriptional regulation, DNA binding and cytoskeleton dynamics. Further functional studies on Vimentin (VIM), a type III intermediate filament protein involved in cytoskeleton organization and cell motility, revealed that PIAS1 exerts its effects on cell migration and cell invasion through the SUMOylation of VIM at Lys-439 and Lys-445 residues. VIM SUMOylation was necessary for its dynamic disassembly, and cells expressing a non-SUMOylatable VIM mutant showed reduced levels of proliferation and migration. Our approach not only provides a novel strategy for the identification of E3 SUMO ligase substrates, but also yields valuable biological insights into the unsuspected role of PIAS1 and VIM SUMOylation on cell motility.

2020-02-06 | PXD011932 | Pride

Trancriptomic profiling of HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi

Project description:To investigate the influence of PBRM1 on gene expression, we performed RNA-seq in HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi (both shRNA and siRNA approaches were used), and identified differentially expressed genes in PBRM1 knock-down cells compared to control cells, which shows implications for PBRM1's biological function in colon cancer.

2018-01-30 | E-MTAB-5566 | biostudies-arrayexpress

Genome wide analysis of transcriptome modification after re-expression of PBRM1 WT and its BAH domain mutant in PBRM1 CRISPR-KO HEK293T cells.

Project description:Purpose: To find out if cancer-associated mutation in BAH domain affects gene expression? Method: We used PBRM1 CRISPR KO HEK293T cells and ectopically expressed GFP-PBRM1-WT, GFP-PBRM1 P1048R, GFP-PBRM1 T1202K and GFP-PBRM1 C1233W plasmid for 48 hours. Result: We found that GFP-PBRM1 WT and GFP-PBRM1 T1202K mutant were identical in terms of gene expression. However, mutant P1048R and C1233W had very little difference in expression of only 15 (14 up- and 1 down) out of 10,160 genes.

2021-09-20 | GSE149874 | GEO

Genome-wide chromatin profiles of PBRM1 [RNA-Seq]

Project description:PBRM1 is an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler. The inactivation of PBRM1 is the second most frequent mutational event in kidney tumorigenesis. Here we show that in VHL-deficient ccRCC tumors, PBRM1 loss results in an altered PBAF complex that retains the association between SMARCA4 and ARID2 but disengages BRD7 from SMARCA4. The PBRM1-deficient PBAF complexes redistribute from promoter proxy regions to distal enhancer regions. The ATPase function of SMARCA4 enhances the recruitment of nuclear factor RELA to aberrant sites and promotes NF-κB activity. Proteasome inhibitor bortezomib reverses NF-κB activation by reducing RELA binding at regions bound by PBRM1-deficient PBAF and delays PBRM1-deficient tumor growth. In conclusion, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-tumorigenic NF-κB target genes by residual PBRM1-deficient PBAF complexes.

2023-02-13 | GSE152734 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data