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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

ABSTRACT: Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

PROVIDER: PRJNA680028 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR13106217.fastq.gz	Fastqsanger.gz
	SRR13106218.fastq.gz	Fastqsanger.gz
	SRR13106219.fastq.gz	Fastqsanger.gz
	SRR13106220.fastq.gz	Fastqsanger.gz
	SRR13106221_1.fastq.gz	Fastqsanger.gz

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

Project description:Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

Project description:To identify which genes are regulated by KLF5 and its acetylation, we performed RNA-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

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Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

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KLF5 co-immunoprecipitation mass spectrometry

Project description:Lineage plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and contributes to tumor heterogeneity and therapeutic resistance. Here, we identify KLF5 as a dynamic master regulator of epithelial lineage identity in PDAC, with dichotomous roles in promoting either classical or basal-like transcriptional programs. Through unbiased proteomic and genetic screens, we uncover the AAA+ ATPases RUVBL1 and RUVBL2 as essential coactivators of KLF5 across both lineage states. We demonstrate that ATP hydrolysis by RUVBL1/2 is required for the stable interaction with an intrinsically disordered region of KLF5, enabling its recruitment to lineage-specific enhancers and driving transcriptional regulation of identity-defining genes. Notably, small-molecule inhibitors of RUVBL1/2 ATPase activity, which have anti-PDAC activity in vivo, suppress KLF5-dependent transcription. These findings define a previously unrecognized mechanism of ATP hydrolysis-dependent transcriptional coactivation by AAA+ ATPases and highlight a potential therapeutic strategy for modulating aberrant lineage programs in cancer. This project contains files relative to a Co-IP MS with KLF5-MBP as bait.

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Tissue microenvironment shapes distinct sets of machineries to regulate ILC2 properties

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Project description:Krüppel-like factors (Klfs) are DNA-binding transcriptional factors that regulate multiple physiological features, including the cell cycle, cell differentiation and tissue organization. Klf2, Klf4 and Klf5 are crucial for maintenance of pluripotent and somatic stem cells. We show that Klf2, Klf4 and Klf5 genes are required for normal neural development in a redundant manner and depletion of all three genes in neural precursor cells results in impaired activation of Notch signaling and early lethality. Klf5 plays a dominant role in maintenance of neural precursor cell populations by suppressing their differentiation and radial migration in developing mammalian brain. Klf4 and Klf5 also regulate proliferation of neural precursor cells in an opposing fashion. Klf4 promotes generation of quiescent neural stem cells, whereas Klf5 supports vigorously dividing intermediate progenitor cells. Our findings provide insight into mechanisms by which neural precursor cells provide large numbers of differentiating cells and a few quiescent neural stem cells.

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