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Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - ChIPseq data

ABSTRACT: Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - ChIPseq data

PROVIDER: PRJNA548800 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9298881.fastq.gz	Fastqsanger.gz
	SRR9298882.fastq.gz	Fastqsanger.gz
	SRR9298884.fastq.gz	Fastqsanger.gz
	SRR9298885.fastq.gz	Fastqsanger.gz
	SRR9298886.fastq.gz	Fastqsanger.gz

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Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq

Project description:Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq

| PRJNA548792 | ENA

Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - ChIPseq data

Project description:In order to identify direct gene targets and pathways regulated by MEIS1 in prostate cells and identify mechanisms of observed tumor suppression with MEIS1 expression, we performed Chromatin Immunoprecipitation and sequencing (ChIP-seq) of MEIS1 in the CWR22Rv1-LV-MEIS1 line. Also, given the dependence of HOXB13, and to enable determination of HOXB13-dependent vs. HOXB13-independent MEIS1 DNA binding, we performed parallel MEIS1 ChIP-seq in the CWR22Rv1-HOXB13ko-LV-MEIS1 line. LV-MEIS1 denotes cells with exogenous lentiviral expression of MEIS1, and they still express endogenous HOXB13. Knockout of HOXB13 was achieved by CRISPR and validated with western blotting. HOXB13ko-LV-MEIS1 denotes cells where the same lentiviral expression of MEIS1 was infected into the HOXB13ko cells, so these cells are positive for MEIS1 expression and negative for HOXB13.

2020-07-15 | GSE132716 | GEO

Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - RNAseq data

Project description:Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - RNAseq data

| PRJNA548764 | ENA

Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq - RNAseq data

Project description:We conducted RNA-sequencing to determine MEIS1-mediated gene regulation in prostate cancer cells because phenotypic data has demonstrated that expression of MEIS1 is sufficient to slow tumor growth and metastatic colonization in vitro and in vivo. These analyses compared global gene expression of CWR22Rv1-Control and CWR22Rv1-LV-MEIS1, as well as the HOXB13ko and HOXB13ko-LV-MEIS1 cells to precisely delineate MEIS1 and HOXB13-regulated genes. Importantly, inclusion of HOXB13ko lines enabled determination of HOXB13-associated gene regulation, as well as identification of significant changes between LV-MEIS1 vs. Control that are HOXB13-independent and thus unrelated to tumor suppression. Are samples are from CWR-22Rv1 cells. Control denotes cells with constitutive expression of Cas9, but with no gRNA provided. Control cells have nearly undetectable levels of endogenous MEIS1 expression, but do express HOXB13. LV-MEIS1 denotes cells with exogenous lentiviral expression of MEIS1, and they still express endogenous HOXB13. HOXB13ko denotes cells where HOXB13 was knocked out using CRISPR, 6 cell clones were isolated with confirmed HOXB13 knockout by western blot and pooled together into one line, so these cells lack both MEIS1 and HOXB13. HOXB13ko-LV-MEIS1 denotes cells where the same lentiviral expression of MEIS1 was infected into the HOXB13ko cell pool, so these cells are positive for MEIS1 expression and negative for HOXB13.

2020-07-15 | GSE132694 | GEO

MEIS1 ChIPseq in CHRF-288-11

Project description:MEIS1 ChIPseq in CHRF-288-11

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Deciphering molecular mechanisms of MEIS1-mediated prostate tumor suppression through RNAseq and ChIPseq

Project description:This SuperSeries is composed of the SubSeries listed below.

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MEIS1 ChIPseq in CHRF-288-11

Project description:ChIP-seq of MEIS1 in the human megakaryocytic cell line CHRF-288-11

2012-01-04 | E-MTAB-859 | biostudies-arrayexpress

Meis1 genomics

Project description:Meis1 function in leukemogenesis

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Meis1 coordinates a network of genes implicated in eye development and microphthalmia

Project description:Microphthalmos is a rare congenital anomaly characterized by reduced eye size and visual deficits of variable degrees. Sporadic and hereditary microphthalmos has been associated to heterozygous mutations in genes fundamental for eye development. Yet, many cases are idiopathic or await the identification of molecular causes. Here we show that haploinsufficiency of Meis1, a transcription factor with an evolutionary conserved expression in the embryonic trunk, brain and sensory organs, including the eye, causes microphthalmic traits and visual impairment, in adult mice. In the trunk, Meis1 acts as a cofactor for genes of the Hox complex, mostly binding to Hox-Pbx target sequence on the DNA. By combining the analysis of Meis1 loss-of-function and conditional Meis1 functional rescue with ChIPseq and RNAseq approaches, we show that during the development of the optic cup, an Hox-free region, Meis1 binds instead to Hox/Pbx-independent Meis binding site, and coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating the expression of components of the Notch signalling pathway. Meis1 also controls the activity of genes responsible for human microphthalmia and eye patterning so that in Meis1-/- embryos, the eye size is reduced and boundaries among the different eye territories are shifted or blurred. We thus propose that Meis1 is at the core of a genetic network implicated in microphthalmia, itself representing an additional candidate for syndromic cases of these ocular malformations. Transcriptomics and Meis1 Occupancy analysis on mouse isolated optic cups and ChIP data for histone methylation marks were obtained from about 100 eyes of E10.5 CD1 embryos.

2015-08-27 | E-GEOD-62786 | biostudies-arrayexpress

Meis1 coordinates a network of genes implicated in eye development and microphthalmia

2015-08-27 | GSE62786 | GEO