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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE137036 | GEO | 2021/09/22

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 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.

2021-10-20 | GSE186005 | GEO

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

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

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Identifying targets of Klf2, Klf4, Klf5 and p53 in mouse embryonic stem cells

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

2010-06-25 | E-GEOD-9535 | biostudies-arrayexpress

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

Genome-wide mapping of Klf4 and Klf5 in pluripotent mouse embryonic stem cells (ESCs)

Project description:We identified the binding profile of Klf4 and Klf5, which are both transcription facyors involved in the maintenance of pluripotency of ESCs by inhibiting their differentiation either into endoderm or mesoderm respectively. Undifferentiated mouse ESCs were used to identify Klf4 and Klf5 bidning sites

2014-04-25 | E-GEOD-49848 | biostudies-arrayexpress

Genomic alterations activating KLF5 [RNA-Seq]

Project description:Using RNA-seq to identify genes that regulated by KLF5 and KLF5 mutants

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WT vs Klf5 KO ES

Project description:Homozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krüppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis Keywords: cell type comparison

2008-12-31 | GSE9244 | GEO

Expression data from conditional Klf5 knockout Pten-null mouse prostates

Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array

2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress

Differential gene expression in intestinal mouse crypts after loss of KLF5

Project description:To determine potential targets of KLF5 we performed RNA-sequencing on jejunal crypts isolated from Klf5-deficient and wildtype mice, using three biological replicates per genotype. We identified 1,480 genes that showed significant differential expression with at least a 2-fold difference between Klf5-deficient and wildtype (q-value â¤ 0.05) (Figure 5A; Supplementary Table 1). Klf5 expression was significantly downregulated 2.7-fold. Comparison of gene expression after loss of KLF5 in the intestine. Isolated jejunal crypts from 3 wildtype and 3 knockout animals were compared.

2016-04-01 | E-GEOD-79758 | biostudies-arrayexpress

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