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

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

PROVIDER: PRJNA680029 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13106240.fastq.gz	Fastqsanger.gz
	SRR13106241.fastq.gz	Fastqsanger.gz
	SRR13106242.fastq.gz	Fastqsanger.gz
	SRR13106243.fastq.gz	Fastqsanger.gz
	SRR13106244.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 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

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

2020-12-19 | GSE161949 | GEO

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

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

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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.

2020-12-19 | GSE161950 | GEO

Klf5 OE ES

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.

2024-10-11 | GSE245044 | GEO

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

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

2020-12-18 | GSE161951 | GEO

KLF5 governs sphingolipid metabolism and barrier function of the skin

Project description:Stem cells are fundamental units of tissue remodeling, whose functions are dictated by lineage-specific transcription factors. Home to epidermal stem cells and their upward stratifying progenies, skin relies upon its secretory functions to form the outmost protective barrier, of which a transcriptional orchestrator has been elusive. KLF5 is a Krüppel-like transcription factor broadly involved in development and regeneration, whose lineage specificity, if any, remains unclear. Here we report KLF5 specifically marks the epidermis, and its deletion leads to skin barrier dysfunction in vivo. Lipid envelopes and secretory lamellar bodies are defective in KLF5-deficient skin, accompanied by preferential loss of complex sphingolipids. KLF5 binds to and transcriptionally regulates genes encoding rate-limiting sphingolipid metabolism enzymes. Remarkably, skin barrier defects elicited by KLF5 ablation can be rescued by dietary interventions. Finally, we found KLF5 is widely suppressed in human diseases with disrupted epidermal secretion, and its regulation of sphingolipid metabolism is conserved in human skin. Altogether, we establish KLF5 as a disease-relevant transcription factor governing sphingolipid metabolism and barrier function in the skin, likely representing a long-sought secretory lineage defining factor across tissue types.

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Over-expression and knockdown of KLF5

Project description:Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. To this end, we manipulated KLF5 expression in four Ras-mutant human lung adenocarcinoma cell lines to find that KLF5 significantly modulates anchorage-independent growth, a mutant Ras phenotype. However, in a mouse model of human lung adenocarcinoma, K-RasG12D does not critically require Klf5 to mediate oncogenesis or induce cyclin D1 expression. Patients with lung tumors expressing high levels of KLF5 have significantly better prognosis than those with low or no KLF5 expression (opposite of mutant Ras prognosis). The latter may be explained by KLF5 transcriptional repression of the ATP-binding cassette, sub-family G (WHITE), member 2 (ABCG2), an anthracycline transporter. In agreement with this, KLF5 knockdown cells display significantly more Hoechst “side population” and resistance to doxorubicin. In summary, while KLF5 is not an obligate partner in Ras oncogenic signaling, KLF5 control of ABCG2 expression is significant to patient survival.

2010-06-23 | GSE16555 | GEO

ChIP-Seq experiments of KLF5, GATA4 and GATA6 in YCC3/AGS/KATOIII cell lines

Project description:Three transcription factors KLF5, GATA4 and GATA6 are recurrently amplified in multiple gastric cancer cohorts, representing one type of lineage-survival oncogenes in gastric cancer. ChIP-Seq analysis of these three factors in multiple cell lines revealed that significant number of genomic sites are co-occupied by KLF5 and GATA4 and/or GATA6. Integrative analysis of ChIP-Seq and gene expression identified several targets of the three transcription factors in both cell lines and primary tumors, including HNF4A. These results suggest that KLF5, GATA4 and GATA6 interact and co-operate to regulate HNF4A and other genes to promote tumorigenesis in gastric cancer. ChIP-Seq experiments of KLF5, GATA4 and GATA6 were performed in three gastric cancer cell lines YCC3, AGS and KATOIII

2014-09-05 | E-GEOD-51705 | biostudies-arrayexpress

KLF5 and BRD4 Cut and Tag in WT U2OS and KLF5-/- U2OS cells

Project description:Cut and tag experiments to determine the binding sites of BRD4 and KLF5 in the presence and absence of KLF5 in U2OS cells

2024-12-09 | E-MTAB-14079 | biostudies-arrayexpress