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Comparision of Psip1/p75 binding and Mll1 binding sites on Hox and non-Hox genes

ABSTRACT: Psip1/p75 binds to Hox genes and colocalizes with Mll1 and in Psip1 KO MEFs Mll1 occupancy is reduced over Hox genes

ORGANISM(S): Mus musculus

PROVIDER: GSE49179 | GEO | 2014/06/27

SECONDARY ACCESSION(S): PRJNA213239

REPOSITORIES: GEO

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Comparision of Psip1/p75 binding and Mll1 binding sites on Hox and non-Hox genes

Project description:Psip1/p75 binds to Hox genes and colocalizes with Mll1 and in Psip1 KO MEFs Mll1 occupancy is reduced over Hox genes Psip1/p75 ChIP using A300-848 abtibody (recognises p75 isoform of Psip1) and Mll1 ChIP from WT and Psip1 KO MEFs ChIP-chip

2014-06-27 | E-GEOD-49179 | biostudies-arrayexpress

Comparision of Psip1/p75, Mll and Menin binding on the Hox and non-Hox genes

Project description:Menin binding pattern in WT and Psip1 KO MEFs Menin occupancy is studied over Hox genes Menin ChIP from WT and Psip1 KO MEFs ChIP-chip

2014-06-27 | E-GEOD-49180 | biostudies-arrayexpress

Comparision of Psip1/p75, Mll and Menin binding on the Hox and non-Hox genes

Project description:Menin binding pattern in WT and Psip1 KO MEFs Menin occupancy is studied over Hox genes

2014-06-27 | GSE49180 | 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

Psip1/p75 restrains Hox gene expression by recruiting both trithorax and polycomb group proteins

Project description:Psip1/p75 restrains Hox gene expression by recruiting both trithorax and polycomb group proteins

| PRJNA213236 | ENA

Comparision of Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II binding on Hox and non-Hox genes

Project description:Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II binding pattern in WT and Psip1 KO MEFs Menin occupancy is studied over Hox genes and several non-hox genes Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II ChIPs from WT and Psip1 KO MEFs

2014-06-27 | E-GEOD-49181 | biostudies-arrayexpress

Comparision of Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II binding on Hox and non-Hox genes

Project description:Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II binding pattern in WT and Psip1 KO MEFs Menin occupancy is studied over Hox genes and several non-hox genes

2014-06-27 | GSE49181 | GEO

LEDGF/p75 is Dispensable for Hematopoiesis but Essential for MLL-rearranged Leukemogenesis

Project description:Mixed-lineage leukemia (MLL) represents a genetically distinct and aggressive subset of human acute leukemia carrying chromosomal translocations of the MLL gene. These translocations result in oncogenic fusions that mediate aberrant recruitment of transcription machinery to MLL target genes. The N-terminus of MLL and MLL-fusions form a complex with Lens Epithelium-Derived Growth Factor (LEDGF/p75; encoded by the Psip1 gene) and MENIN. This complex contributes to the association of MLL and MLL-fusion multiprotein complexes with chromatin. Several studies have shown that both MENIN and LEDGF/p75 are required for efficient MLL fusion-mediated transformation and for the expression of downstream MLL-regulated genes like HOXA9 and MEIS1. In light of the development of a therapeutic strategy targeting this complex, understanding the function of LEDGF/p75 in normal hematopoiesis is crucial. We generated a conditional Psip1 knockout mouse model in the hematopoietic compartment and examined the effects of LEDGF/p75 depletion in postnatal hematopoiesis and the initiation of MLL leukemogenesis. Psip1 knockout mice were viable but showed several defects in hematopoiesis, reduced colony-forming activity in vitro, decreased expression of Hox genes in hematopoietic stem cells and decreased MLL occupancy at MLL target genes. Finally, in vitro and in vivo experiments showed that LEDGF/p75 is dispensable for steady state hematopoiesis but essential for the initiation of MLL-mediated leukemia. These data corroborate the MLL-LEDGF/p75 interaction as novel target for the treatment of MLL-rearranged leukemia.

2017-09-30 | GSE104138 | GEO

Mus musculus

Project description:Comparision of Psip1/p75 binding and Mll1 binding sites on Hox and non-Hox genes

| PRJNA213239 | ENA

Expression analysis on Mll1+/+ and Mll1-/- MEFs

Project description:Global analysis of H3K4 methylation defines MLL family member targets and points to a role for MLL1-mediated H3K4 methylation in the regulation of transcriptional initiation by RNA polymerase II A common landmark of activated genes is the presence of trimethylation on lysine 4 of histone H3 (H3K4) at promoter regions. The Set1/COMPASS was the founding member and the only H3K4 methylases in S. cerevisiae, however, in mammals at least six H3K4 methylases Set1A/B and MLL1-4 are found in COMPASS-like complexes capable of methylating H3K4. To gain further insight into the different roles and functional targets for the H3K4 methylases, we have undertaken a genome-wide analysis of H3K4 methylation pattern in wild-type Mll1+/+ and Mll1-/- mouse fibroblasts (MEFs). We found that Mll1 is required for the H3K4 trimethylation of less than 5% of promoters carrying this modification. Many of these genes, which include developmental regulators such as Hox genes show decreased levels of RNA polymerase II recruitment and expression concomitant with the loss of H3K4 methylation. Although Mll1 is only required for the methylation of a subset of Hox genes, Menin, a component of the Mll1 and Mll2 complexes, is required for the overwhelming majority of H3K4 methylation at Hox loci. However, the loss of MLL3/4 and/or the Set1 complexes have little to no effect on the Hox loci H3K4 methylation or expression levels in these MEFs. Together these data provide insight into redundancy and specialization of COMPASS-like complexes in mammals and provide evidence on a possible role for Mll1-mediated H3K4 methylation in the regulation of transcriptional initiation. Expression arrays were done with Mll1+/+ and Mll1-/- mouse embryonic fibroblasts. Four replicates were done (dyes were swapped). DNA was hybridized to Agilent Mouse Whole Genome Expression Arrays (4x44k).

2009-10-20 | E-GEOD-18261 | biostudies-arrayexpress

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