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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [CUT&RUN]

ABSTRACT: Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [CUT&RUN]

PROVIDER: PRJNA1251688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33163500_1.fastq.gz	Fastqsanger.gz
	SRR33163500_2.fastq.gz	Fastqsanger.gz
	SRR33163501_1.fastq.gz	Fastqsanger.gz
	SRR33163501_2.fastq.gz	Fastqsanger.gz
	SRR33163502_1.fastq.gz	Fastqsanger.gz

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [Xenium]

Project description:To investigate the role UTX (KDM6A) in stratifying epithelia

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [Xenium]

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [RNA-seq]

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [ChIP-seq]

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [CUT&RUN]

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [RNA-seq]

Project description:Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [RNA-seq]

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Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [ChIP-seq]

Project description:Utx (Kdm6a) promotes differentiation non-catalytically in somatic self-renewing epithelia [ChIP-seq]

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Alternative mRNA splicing controls functions of the human H3K27 demethylase UTX/KDM6A

Project description:The UTX/KDM6A gene encodes the UTX histone H3K27 demethylase, which plays an important role in mammalian development and is frequently mutated in cancers and particularly, in urothelial cancers. Using BioID technique, we explored the interactome of different UTX isoforms.

2024-01-28 | PXD041254 | Pride

Small Cell Lung Cancer Subtype Plasticity is Regulated by KDM6A/UTX [RNA-Seq]

Project description:Using a CRISPR-based autochthonous SCLC GEMM to study the consequences of KDM6A/UTX inactivation, we found that KDM6A inactivation induced plasticity from ASCL1 to NEUROD1 resulting in SCLC tumors with open chromatin at the NEUROD1 promoter that express both ASCL1 and NEUROD1. Mechanistically, KDM6A binds and maintains ASCL1 target genes in an active chromatin state with its loss increasing H3K27me3 near their promoters leading to a cell state that is primed for ASCL1 to NEUROD1 subtype switching. This work identifies KDM6A as an epigenetic regulator that controls ASCL1 to NEUROD1 subtype plasticity and provides a novel autochthonous SCLC GEMM to model ASCL1 and NEUROD1 subtype heterogeneity and plasticity, which is found in 35-40% of human SCLCs.

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Small Cell Lung Cancer Subtype Plasticity is Regulated by KDM6A/UTX [ChIP-Seq]

Project description:Using a CRISPR-based autochthonous SCLC GEMM to study the consequences of KDM6A/UTX inactivation, we found that KDM6A inactivation induced plasticity from ASCL1 to NEUROD1 resulting in SCLC tumors with open chromatin at the NEUROD1 promoter that express both ASCL1 and NEUROD1. Mechanistically, KDM6A binds and maintains ASCL1 target genes in an active chromatin state with its loss decreasing H3K4me1 and increasing H3K27me3 at enhancers of neuroendocrine genes leading to a cell state that is primed for ASCL1 to NEUROD1 subtype switching. This work identifies KDM6A as an epigenetic regulator that controls ASCL1 to NEUROD1 subtype plasticity and provides a novel autochthonous SCLC GEMM to model ASCL1 and NEUROD1 subtype heterogeneity and plasticity, which is found in 35-40% of human SCLCs.

2023-06-09 | GSE228345 | GEO

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