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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [RNA-Seq]

ABSTRACT: Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [RNA-Seq]

PROVIDER: PRJNA793900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17415451.fastq.gz	Fastqsanger.gz
	SRR17415452.fastq.gz	Fastqsanger.gz
	SRR17415453.fastq.gz	Fastqsanger.gz
	SRR17415454.fastq.gz	Fastqsanger.gz
	SRR17415455.fastq.gz	Fastqsanger.gz

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [ChIP-Seq]

Project description:Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [ChIP-Seq]

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [CUT&TAG]

Project description:Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [CUT&TAG]

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [CUT&TAG]

Project description:We performed multiomic high-throughput sequencing to recapitulated the primary mechanism of mesenchymal stem cells osteogenesis. We analysed the H3K27ac ChIP-seq, BRD4 CUT&Tag and RNA-seq data before and after osteogenesis, and identified super enhancers (SEs) regulated osteogenic identity genes in MSCs.

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [RNA-Seq]

Project description:We performed multiomic high-throughput sequencing to recapitulated the primary mechanism of mesenchymal stem cells osteogenesis. We analysed the H3K27ac ChIP-seq and RNA-seq data before and after osteogenesis, and identified super enhancers (SEs) regulated osteogenic identity genes in MSCs.

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [ChIP-Seq]

Project description:We performed multiomic high-throughput sequencing to recapitulated the primary mechanism of mesenchymal stem cells osteogenesis. We analysed the H3K27ac ChIP-seq and RNA-seq data before and after osteogenesis, and identified super enhancers (SEs) regulated osteogenic identity genes in MSCs.

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16

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

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Zbtb16 regulates social cognitive behaviors and neocortical development

Project description:Recent genomic studies suggest that a single gene is involved in multiple diseases, however it is unclear what mechanism destined for different diseases by a single gene. Mutations of ZBTB16 are associated with autism spectrum disorder (ASD) and schizophrenia (SCZ), but how ZBTB16 fates ASD or SCZ are unknown. Here we show the deletion of Zbtb16 in mice leads to both ASD- and SCZ-like behaviors such as social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we carried out histological studies and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in the prefrontal cortex (PFC) of Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia as well as developmental defects in oligodendrocytes and neocortical myelination in the PFC of Zbtb16 KO mice. Using a genomics approach, we identified the Zbtb16-transcriptome that includes genes involved in both ASD and SCZ pathophysiology and neocortical maturation such as neurogenesis and myelination. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ respectively. Our study provides insight into the differential role of the single gene ZBTB16 in ASD and SCZ.

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ZBTB16 inhibits DNA replication and induces cell cycle arrest by targeting WDHD1 transcription in lung adenocarcinoma [ChIP-seq]

Project description:Lung adenocarcinoma is a malignant tumor with high morbidity and mortality. ZBTB16 plays a double role in various tumors; however, the potential mechanism of ZBTB16 in the pathophysiology of lung adenocarcinoma has yet to be elucidated. We herein observed a decreased expression of ZBTB16 mRNA and protein in lung adenocarcinoma and a significantly increased DNA methylation level of ZBTB16 in patients with lung adenocarcinoma. Analysis of public databases and patients’ clinical data indicated a close association between ZBTB16 and patient survival. Ectopic expression of ZBTB16 in lung adenocarcinoma cells significantly inhibited cell proliferation, invasion, and migration. It also induced cell cycle arrest in the S phase. Meanwhile, mitotic catastrophe was induced, and DNA damage and apoptosis occurred. In line with these findings, the overexpression of ZBTB16 in xenograft mice resulted in the inhibition of tumor growth. Comprehensive analysis showed that WDHD1 was a potential target for ZBTB16. The overexpression of both isoforms of WDHD1 significantly reversed the ZBTB16-mediated inhibition of lung adenocarcinoma proliferation and cell cycle. These studies suggest that ZBTB16 impedes the progression of lung adenocarcinoma by interfering with WDHD1 transcription, making it a potential novel therapeutic target in the management of lung adenocarcinoma.

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