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Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

ABSTRACT: The aim of this experiment was to investigate the dysregulation of gene expression in whole E12.5 embryos containing a gene trap (CH) or point mutation (H275R) within the Klf3 gene Affymetrix microarrays were performed on RNA from wildtype, Klf3 H275R/H275R, Klf3 H275R/+, Klf3 CH homozygous and Klf3 CH heterozygous E12.5 embryos

ORGANISM(S): Mus musculus

PROVIDER: GSE43908 | GEO | 2013/01/31

SECONDARY ACCESSION(S): PRJNA188166

REPOSITORIES: GEO

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Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

Project description:The aim of this experiment was to investigate the dysregulation of gene expression in whole E12.5 embryos containing a gene trap (CH) or point mutation (H275R) within the Klf3 gene Affymetrix microarrays were performed on RNA from wildtype, Klf3 H275R/H275R, Klf3 H275R/+, Klf3 CH homozygous and Klf3 CH heterozygous E12.5 embryos Four wildtype replicates, three Klf3 H275R/H275R replicates, four Klf3 H275R/+ replicates, four Klf3 CH homozygous replicates and two Klf3 CH heterozygous replicates of whole E12.5 embryos, litter-matched where possible.

2013-01-31 | E-GEOD-43908 | biostudies-arrayexpress

Mus musculus

Project description:Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

| PRJNA188166 | ENA

Microarray analysis of wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt TER119+ E13.5 fetal liver cells

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Microarray analysis of wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt TER119+ E13.5 fetal liver cells

Project description:The aim of this experiment was to investigate the regulation of gene expression by KLF3 and KLF8 in fetal erythroid cells by analyzing single and double mutant mouse models. Affymetrix microarrays were performed on RNA from TER119+ fetal liver cells from E13.5 wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt mice. Four wildtype replicates, four Klf8gt/gt replicates, three Klf3-/- replicates and four Klf3-/- Klf8gt/gt replicates of E13.5 TER119+ fetal liver cell samples, litter-matched where possible.

2013-01-17 | E-GEOD-43524 | biostudies-arrayexpress

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [RNA-seq]

Project description:The differentiated layers of the epidermis protect the body from the outside environment. Impairments in the differentiation process can lead to skin diseases that can afflict ~20% of the population. Thus, it is of utmost importance to characterize and understand the factors that promote the differentiation process. Here we identify the transcription factor KLF3 as a novel regulator of epidermal differentiation. Knockdown of KLF3 results in reduced differentiation gene expression and increased cell cycle gene expression. Over 50% of KLF3’s genomic binding sites occur at regions containing H3K4me/H3K27ac with the vast majority at active enhancers. KLF3 bound to active enhancers proximal to differentiation genes that are dependent upon KLF3 for expression. Based on this association, we sought to investigate KLF3’s possible relationship with the enhancer associated proteins CBP and P300. Analysis of the transcriptome controlled by CBP and P300 showed that CBP and KLF3 control a similar gene expression program and are both essential for promoting differentiation. In addition, 35% of CBP’s genomic binding sites overlap with KLF3 and knockdown of KLF3 results in reduced CBP localization at enhancers proximal to differentiation gene clusters. Our results suggest that KLF3 regulates differentiation gene expression by promoting CBP localization at enhancers.

2020-07-22 | GSE140990 | GEO

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [ChIP-seq]

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Expression data of K562 cells with KLF3 deficiency and shRNA vector control

Project description:KLF3, a member of the Krüppel-like factor (KLF) family, is expressed in a wide range of cell types. It is involved in hematopoiesis of several blood cell lineages including erythrocyte and B lymphocyte. However, the research of regulatory roles on hematopoiesis of KLF3 in K562 cells has been still largely limited. To comprehensively assess the regulatory roles of KLF3 on hematopoiesis in K562 cells, a microarray analysis was performed in KLF3-deficient K562 cells. The differentially expressed genes were applied to IPA analysis to observe the perturbed hematopoiesis-associated functions, networks, and molecular pathways. This study will extensively assess the regulatory roles of KLF3 on hematopoiesis in K562 cells. We used microarrays to study the genome-wide expression profiles of KLF3-deficient K562 cells.

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Programming of marginal zone B cell fate by basic krüppel-like factor (BKLF/KLF3)

Project description:Gene expression analysis of splenic follicular B cells and marginal zone B cells from B6 and CD19:KLF3 transgenic mice Comparing KLF3-transgenic and non-transgenic follicular B cells by RNA-microarray revealed that KLF3 regulates a subset of genes that was similarly up-/downregulated upon normal MZ B cell differentiation. Indeed, KLF3 expression overcame the lack of MZ B cells caused by different genetic alterations, such as CD19-deficiency or blockade of B-cell activating factor (BAFF)-receptor signaling, indicating that KLF3 may complement alternative NF-κB signaling. Thus, KLF3 is a driving force towards MZ B cell maturation.

2011-01-29 | GSE26948 | GEO

Gene expression data from WT and Klf3 KO mouse CD19+ splenic B cells

Project description:To investigate the roles of Klf3 in B lymphopoiesis, CD19+ B cells were sorted from the spleens of WT and Klf3 KO mice (Molecular and Cellular Biology (2008); 28:3967–3978). Following RNA extraction, gene expression was compared in WT and Klf3 KO CD19+splenic B cells using Affymetrix microarrays.

2011-08-26 | GSE31622 | GEO

Genome-wide binding profiles of KLF3 and KLF3 mutants in MEF cells

Project description:Transcription factors are often regarded as being comprised of a DNA-binding domain and a functional domain. The two domains are considered separable and autonomous, with the DNA-binding domain directing the factor to its target genes and the functional domain imparting transcriptional regulation. We have examined a typical Zinc Finger (ZF) transcription factor from the Krüppel-like factor (KLF) family, KLF3. This factor has an N-terminal repression domain that binds the co-repressor C-terminal binding protein (CtBP), and a DNA-binding domain composed of three classical (ZFs) at its C-terminus. We established a system to compare the genomic occupancy profile of wildtype KLF3 with two mutants affecting the N-terminal functional domain: a mutant unable to contact its cofactor CtBP and a mutant lacking the entire N-terminal domain, but retaining the ZFs intact. We used chromatin immunoprecipitation followed by sequencing (ChIP-seq) to assess binding across the genome in murine embryonic fibroblasts. Our results define the in vivo recognition site for KLF3 and the two mutants as a typical CACCC-like element. Unexpectedly, we observe that mutations in the N-terminal functional domain severely affect DNA binding. In general, both mutations reduce binding but there are also instances where binding is retained or even increased. These results provide a clear demonstration that the correct localization of transcription factors to their target genes is not solely dependent on their DNA-contact domains. This informs our understanding of how transcription factors operate and is of relevance to the design of artificial ZF proteins. ChIP-seq was performed on the three samples, KLF3, ΔDL and DBD in duplicate (biological replicates). Input samples were used as controls.

2013-10-17 | E-GEOD-44748 | biostudies-arrayexpress

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