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Klf5 confers embryonic and extra-embryonic bi-potential cell fate in early blastomeres and embryonic stem cells

ABSTRACT: This study examines the transcriptomes of embryonic stem cells following overexpression of Klf5. Additionally, this study examines the transcripomes of single embryos either treated with scramble siRNA or siRNA targeting Klf5.

ORGANISM(S): Mus musculus

PROVIDER: GSE186005 | GEO | 2021/10/20

REPOSITORIES: GEO

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Klf5 confers embryonic and extra-embryonic bi-potential cell fate in early blastomeres and embryonic stem cells

Project description:This study determines the genome-wide binding profile of a V5-tagged KLF5 transription factor exogenously expressed in mouse embryonic stem cells.

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Klf5 confers embryonic and extra-embryonic bi-potential cell fate in early blastomeres and embryonic stem cells

Project description:Klf5 confers embryonic and extra-embryonic bi-potential cell fate in early blastomeres and embryonic stem cells

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Klf5 confers embryonic and extra-embryonic bi-potential cell fate in early blastomeres and embryonic stem cells

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Effect of Cyclin-dependent kinase 2 (CINP) inhibition on TSU-PR1 cell line with stable KLF5 expression May

Project description:To study wither loss of CINP rescues global gene expression by KLF5 overexpression, we compare the effect of siRNA-mediated CINP silencing on K12 cells (TSU-PR1 cell line with stable KLF5 expression).

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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.

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Project description:This SuperSeries is composed of the following subset Series: GSE9774: Klf2, Klf4, Klf5 and p53 in mouse embryonic stem cells GSE9775: To identify the target genes of Klf2, Klf4 and Klf5 in mouse embryonic stem cells. Keywords: SuperSeries Refer to individual Series

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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.

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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

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Project description:Klf5 OE ES

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