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TXNIP loss expands Myc transcriptome [RNA-seq]

ABSTRACT: To better understand how TXNIP in the contributes to the poor prognosis of triple-negative breast cancers, our lab has generated TXNIP null MDA-MB-231 cells (231:TKO). We characterized the gene exrpession programs of these cells by RNA-seq. To determine the Myc-dependence of the transcriptional programs of 231:TKO cells, we used an siRNA RNA approach to reduce Myc levels.

ORGANISM(S): Homo sapiens

PROVIDER: GSE208415 | GEO | 2023/02/07

REPOSITORIES: GEO

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TXNIP loss expands Myc transcriptome

Project description:To examine the generality of our finding where the gene expression profile of TXNIP knockout in MDA-MB-231 cells resembles of that Myc overexpression transcriptional program, our lab has generated TXNIP null HCC70 (HCC70:TKO) and MB135 (MB135:TKO) cells. We characterized the gene exrpession programs of these cells by RNA-seq.

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TXNIP loss increases Myc genomic occupancy [ChIP-seq]

Project description:Our RNA sequencing result demonstrated that TXNIP loss increased the levels of Myc-dependent transcription. To determine whether TXNIP regulates global Myc genomic occupancy, we performed Myc ChIP-seq on parental 231 and 231:TKO cells.

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TXNIP loss does not increase chromatin accessibility for Myc binding.

Project description:Our Myc ChIP sequencing result demonstrated that TXNIP loss increased Myc genomic occupancy levels. To determine whether TXNIP loss increased Myc genomic occupancy through increasing chromatin accessibility for Myc binding, we performed assay for transposase-accessible chromatin with sequencing (ATAC-seq) on parental 231 and 231:TKO cells.

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BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP

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TXNIP loss increases Myc genomic occupancy [ChIP-seq]

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Project description:Cardiomyocyte specific knock in mouse heart with Txnip Cysteine 247 to Serine Mutation

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