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Chip-chip from Mouse MEFs cells for H3K36me3, Srsf1, Psip1(A300-847 antibody).

ABSTRACT: The p52 isoform of Psip1/Ledgf links histone H3K36 methylation and the regulation of alternative splicing. Chromatin immunoprecipitation (ChIP) of Psip1 together with H3K36me3 and Srsf1 and by ChIP-on-chip analysis demonstrated that H3K36me3, Psip1 and SRSF1 enrichment correlates on the gene bodies

ORGANISM(S): Mus musculus

PROVIDER: GSE31520 | GEO | 2012/01/01

SECONDARY ACCESSION(S): PRJNA145509

REPOSITORIES: GEO

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Chip-chip from Mouse MEFs cells for H3K36me3, Srsf1, Psip1(A300-847 antibody).

Project description:The p52 isoform of Psip1/Ledgf links histone H3K36 methylation and the regulation of alternative splicing. Chromatin immunoprecipitation (ChIP) of Psip1 together with H3K36me3 and Srsf1 and by ChIP-on-chip analysis demonstrated that H3K36me3, Psip1 and SRSF1 enrichment correlates on the gene bodies Array design includes 2 dye swap replicates for Srsf1 and Psip1-/- samples, and single arrays for PSIP and H3K36me3 samples

2012-01-01 | E-GEOD-31520 | biostudies-arrayexpress

Psip1 ChIP using A300-847 antibody (Immunoprecipitates mainly p52 isoform of Psip1) Chip-chip from Mouse MEFs cells with H3K36me3, H3K4me3, Psip1 ChIP using A300-847 antibody

Project description:The p52 isoform of Psip1/Ledgf links histone H3K36 methylation and the regulation of alternative splicing. Chromatin immunoprecipitation (ChIP) of Psip1 together with H3K36me3 and H3K4me3 and by ChIP-on-chip analysis demonstrated that, Like H3K36me3, Psip1 is enriched on exons of highly expressed genes, Comparision of H3K36me3 and Psip1 binding sites on the expressed and non expressed genes.

2012-04-11 | E-GEOD-28153 | biostudies-arrayexpress

Psip1 ChIP using A300-847 antibody (Immunoprecipitates mainly p52 isoform of Psip1) Chip-chip from Mouse MEFs cells with H3K36me3, H3K4me3, Psip1 ChIP using A300-847 antibody

Project description:The p52 isoform of Psip1/Ledgf links histone H3K36 methylation and the regulation of alternative splicing. Chromatin immunoprecipitation (ChIP) of Psip1 together with H3K36me3 and H3K4me3 and by ChIP-on-chip analysis demonstrated that, Like H3K36me3, Psip1 is enriched on exons of highly expressed genes,

2012-04-12 | GSE28153 | GEO

RNAi of human Jurkat cells knocked down LEDGF transcript of PSIP1 gene

Project description:The LEDGF transcript from the PSIP1 gene was knocked down in Jurkat cells using RNAi technology. The resulting Jurkat-derived cell line (Jurkat-siJK2) was compared to a control cell line (wild type Jurkat) using microarray analysis. Genes identified as being modulated by LEDGF were preferential targets of HIV integration. Experiment Overall Design: 2 cell lines were used, Jurkat-siJK2 (experimental) and wild-type Jurkat (control). 3 independent cultures of each cell line were used for independent RNA extractions, labeling reactions and array hybridizations.

2008-06-15 | E-GEOD-7508 | biostudies-arrayexpress

PSIP1/LEDGF reduces R-loops at transcription sites and maintain genome integrity (TT-Seq)

Project description:R-loops are transcriptional by-products that pose a persistent threat to genome integrity and are implicated in accelerated ageing and cancer. PSIP1/LEDGF is a multifunctional chromatin protein that associates with transcriptional elongation machinery. Here, we demonstrated that PSIP1 interacts with R-loops generated at the site of transcription and along with the factors involved in R-loop resolution, including PARP1. Reduced PSIP1 levels in human and mouse cells lead to an increase in R-loop levels and DNA damage at the PSIP1 binding sites. This increased R-loops and DNA damage was specific at the RNA polymerase II transcription sites, causing local transcriptional arrest. In addition, we demonstrate that PSIP1 can be targeted for increasing the sensitivity of cancer cells to PARP1 inhibitors and transcription-coupled DNA damaging agents. These findings show the critical role of PSIP1 in reducing the R-loop burden and DNA damage at the transcriptionally active regions of the genome.

2023-12-08 | GSE220233 | GEO

PSIP1/LEDGF reduces R-loops at transcription sites and maintain genome integrity (RNA-Seq)

2023-12-08 | GSE220232 | GEO

PSIP1/LEDGF reduces R-loops at transcription sites and maintain genome integrity (CUT&Tag-Seq)

2023-12-08 | GSE220231 | GEO

RNAi knock down of LEDGF transcript from the PSIP1 gene in human 293T cells reveals a role for LEDFG/p75 in targeting HIV integration

Project description:The LEDGF transcript from the PSIP1 gene was knocked down using RNAi technology. The resulting 293T derived cell line (293TsiLL) was compared to a control cell line (293TsiScram) using microarray analysis. Genes identified as being modulated by LEDGF were preferential targets of HIV integration. Experiment Overall Design: 2 cell lines were used, 293TsiLL (experimental) and 293TsiScram (control). 4 independent cultures of each cell line were used for independent RNA extractions, labeling reactions and array hybridizations.

2007-10-27 | E-GEOD-3485 | biostudies-arrayexpress

PSIP1/LEDGF reduces R-loops at transcription sites and maintain genome integrity (HEK293T CUT&Tag-Seq)

2023-12-08 | GSE245788 | GEO

PSIP1/p75 promotes tumorigenicity in breast cancer cells by promoting the transcription of cell cycle genes

Project description:Breast cancer (BC) is a highly heterogeneous disease, both at the pathological and molecular level, and several chromatin-associated proteins play crucial roles in breast cancer initiation and progression. Here, we demonstrate the role of PSIP1 (PC4 and SF2 interacting protein)/p75 (LEDGF) in breast cancer progression. PSIP1/p75, previously identified as a chromatin-adaptor protein, is found to be upregulated in basal-like/triple negative breast cancer (TNBC) patient samples and cell lines. Immunohistochemistry in tissue arrays showed elevated levels of PSIP1 in metastatic invasive ductal carcinoma. Survival data analyses indicated that the levels of PSIP1 showed a negative association with TNBC patient survival. Depletion of PSIP1/p75 significantly reduced the tumorigenicity and metastatic properties of TNBC cell lines while its over-expression promoted tumorigenicity. Further, gene expression studies revealed that PSIP1 regulates the expression of genes controlling cell-cycle progression, cell migration, and invasion. Finally, by interacting with RNA polymerase II, PSIP1/p75 facilitates the association of RNA pol II to the promoter of cell cycle genes and thereby regulates their transcription. Our findings demonstrate an important role of PSIP1/p75 in TNBC tumorigenicity by promoting the expression of genes that control the cell cycle and tumor metastasis.

2017-06-06 | GSE99699 | GEO

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