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Role of CASZ1 in keratinocyte differentiation [RNA-seq]

ABSTRACT: Here we indentified CASZ1 as an essential regulator of the epidermal differentiation program.

ORGANISM(S): Homo sapiens

PROVIDER: GSE261518 | GEO | 2024/04/16

REPOSITORIES: GEO

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Role of CASZ1 in keratinocyte differentiation [CUT&RUN]

Project description:Here we indentified CASZ1 as an essential regulator of the epidermal differentiation program.

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Role of CASZ1 in keratinocyte differentiation

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TMT analysis of TBX20:CASZ1 mutant mice with dilated cardiomyopathy

Project description:Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM. Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM.

2022-05-27 | PXD005788 | Pride

Role of CASZ1 in keratinocyte differentiation

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

2024-04-16 | GSE261573 | GEO

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

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mCasz1_conditional knockout

Project description:The overall goal of our studies is to elucidate the cellular and molecular mechanism by which the transcription factor Casz1 functions in murine heart development. We established that Casz1 is expressed in myocardial progenitor cells beginning at E7.5 and in differentiated cardiomyocytes throughout development. We generated conditional Casz1 knockout mice to show that ablation of CASZ1 in Nkx2.5-positive cardiomyocytes leads to cardiac hypoplasia, ventricular septal defects and lethality by E13.5. To identify the pathways and networks by which Casz1 regulates cardiomyocyte development, we used RNA-Seq and identified genes involved in cell proliferation are upregulated in Casz1 mutants compared to wild-type littermates. We conclude that Casz1 is essential for cardiac development and has a pivotal role in regulating part of the cardiac transcriptional program. 3 biological replicates of the two genotypes (Nkx2-5+/+,Casz1f/+ and Nkx2-5Cre/+,Casz1f/f) were used for RNA-seq to determine genes that are differentially expressed in the murine heart when Casz1 is mutated. Nkx2-5+/+,Casz1f/+ were used as wild-type controls for comparison.

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