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CASZ1 is essential for activation of epidermal terminal differentiation

ABSTRACT: CASZ1 is essential for activation of epidermal terminal differentiation

PROVIDER: PRJNA1010404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25782266.fastq.gz	Fastqsanger.gz
	SRR25782267.fastq.gz	Fastqsanger.gz
	SRR25782268.fastq.gz	Fastqsanger.gz
	SRR25782269.fastq.gz	Fastqsanger.gz
	SRR27717500.fastq.gz	Fastqsanger.gz

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CASZ1 is essential for activation of epidermal terminal differentiation

Project description:CASZ1 is a novel and potent activator of terminal epidermal differentiation. CASZ1 knockdown inhibits transcription of the epidermal differentiation program. p63 and p300 are required to activate CASZ1 expression.

2024-02-26 | GSE241873 | GEO

Role of CASZ1 in keratinocyte differentiation [CUT&RUN]

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

2024-04-16 | GSE261527 | GEO

Role of CASZ1 in keratinocyte differentiation [RNA-seq]

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

2024-04-16 | GSE261518 | GEO

CASZ1 Is Essential for Skin Epidermal Terminal Differentiation.

Project description:The barrier function of skin epidermis is crucial for our bodies to interface with the environment. Because epidermis continuously turns over throughout the lifetime, this barrier must be actively maintained by regeneration. Although several transcription factors have been established as essential activators in epidermal differentiation, it is unclear whether additional factors remain to be identified. In this study, we show that CASZ1, a multi zinc-finger transcription factor previously characterized in nonepithelial cell types, shows highest expression in skin epidermis. CASZ1 expression is upregulated during epidermal terminal differentiation. In addition, CASZ1 expression is impaired in several skin disorders with impaired barrier function, such as atopic dermatitis, psoriasis, and squamous cell carcinoma. Using transcriptome profiling coupled with RNA interference, we identified 674 differentially expressed genes with CASZ1 knockdown. Downregulated genes account for 91.2% of these differentially expressed genes and were enriched for barrier function. In organotypic epidermal regeneration, CASZ1 knockdown promoted proliferation and strongly impaired multiple terminal differentiation markers. Mechanistically, we found that CASZ1 upregulation in differentiation requires the action of both the master transcription factor, p63, and the histone acetyltransferase, p300. Taken together, our findings identify CASZ1 as an essential activator of epidermal differentiation, paving the way for future studies understanding of CASZ1 roles in skin disease.

| S-EPMC11344692 | biostudies-literature

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

Epidermal Growth Factor Receptor Activation is Essential for Kidney Fibrosis Development

Project description:Epidermal Growth Factor Receptor Activation is Essential for Kidney Fibrosis Development

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ZNF750 Drives Terminal Epidermal Differentiation via Induction of Klf4

Project description:Disrupted differentiation is a hallmark of numerous diseases, which in epidermis alone impact >25% of the population. In a search for dominant mediators of differentiation, we defined a requirement for the ZNF750 nuclear protein in terminal epidermal differentiation. ZNF750 controlled genes mutated in numerous human skin diseases, including FLG, LOR, LCE3B, ALOXE3, and SPINK5. ZNF750 potently induced progenitor differentiation via an evolutionarily conserved C2H2 zinc finger motif. The epidermal master regulator, p63, bound the ZNF750 promoter and was necessary for its induction. ZNF750 restored differentiation to p63-deficient tissue, suggesting it acts downstream of p63. A search for functionally important ZNF750 targets via analysis of ZNF750-regulated genes identified KLF4, a transcription factor that activates late epidermal differentiation genes. ZNF750 binds the Klf4 promoter and controls its expression. ZNF750 thus provides a direct link between a tissue-specifying factor, p63, and an effector of terminal differentiation, Klf4, and represents a potential future target for disorders of this process. Gene expression analysis: To establish a differentiation signature for primary human keratinocytes, with ZNF750-depleted, and Klf4-depleted, total RNA was isolated in biologic duplicate from cells in different conditions and hybridized to Affymetrix HG-U133 2.0 Plus arrays.

2012-02-15 | E-GEOD-32685 | biostudies-arrayexpress

ZNF750 Drives Terminal Epidermal Differentiation via Induction of Klf4

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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.

2019-12-26 | GSE126143 | GEO

Casz1 is required for both inner hair cell fate stabilization and outer hair cell survival

Project description:Cochlear inner hair cells (IHCs) and outer hair cells (OHCs) require different transcription factors for their cell fate stabilization and survival, suggesting separate mechanisms are involved. Here, we found that the transcription factor Casz1 was crucial for early IHC fate consolidation and for OHC survival during mouse development. Loss of Casz1 resulted in transdifferentiation of IHCs into OHCs, without affecting OHC production. However, long-term OHC survival was compromised in Casz1 mutant mice. In addition, the transcription factor Gata3 was downregulated in Casz1-deleted IHCs and overexpressing Gata3 partially rescued IHC properties, OHC numbers, and hearing in Casz1-deleted mice. Thus, Casz1 plays critical roles in early IHC fate stabilization and OHC survival and could potentially provide a lead for therapies aimed at regenerating both IHCs and OHCs.

2025-02-01 | GSE279618 | GEO

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