Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [RNA-seq]

ABSTRACT: Multipotent progenitors confirm their T-lineage identity at the DN2a to DN2b pro-T cell transition, when expression of the essential transcription factor Bcl11b begins. This study defines the molecular basis of direct and indirect actions of Bcl11b in acquisition of T cell identity. In vivo and in vitro stage-specific deletions identify functional regulation targets genome-wide for mechanistic analysis. Bcl11b can associate with multiple co-factors and its direct action is needed to recruit these to selective target sites. Sites of Bcl11b-dependent cofactor recruitment are enriched at functionally regulated targets, and deletion of individual cofactors can relieve repression of many Bcl11b-repressed genes. In parallel, Bcl11b indirectly regulates a subset of its target genes by a gene network circuit via Id2 and Zbtb16, which are directly repressed by Bcl11b and control distinct alternative programs.

ORGANISM(S): Mus musculus

PROVIDER: GSE110882 | GEO | 2018/09/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

Project description:Multipotent progenitors confirm their T-lineage identity at the DN2a to DN2b pro-T cell transition, when expression of the essential transcription factor Bcl11b begins. This study defines the molecular basis of direct and indirect actions of Bcl11b in acquisition of T cell identity. In vivo and in vitro stage-specific deletions identify functional regulation targets genome-wide for mechanistic analysis. Bcl11b can associate with multiple co-factors and its direct action is needed to recruit these to selective target sites. Sites of Bcl11b-dependent cofactor recruitment are enriched at functionally regulated targets, and deletion of individual cofactors can relieve repression of many Bcl11b-repressed genes. In parallel, Bcl11b indirectly regulates a subset of its target genes by a gene network circuit via Id2 and Zbtb16, which are directly repressed by Bcl11b and control distinct alternative programs.

2018-09-21 | GSE110305 | GEO

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [ChIP-seq]

2018-09-21 | GSE115742 | GEO

BCL11B AND COMBINATORIAL RESOLUTION OF CELL FATE IN THE T-CELL GENE REGULATORY NETWORK

Project description:We report the RNA-seq results from mouse T-cell precursors in different developmental stages including DN1, DN2a, DN2b, DN3 and DP in order to study the gene regulation network in T cell development. Some of the samples also have certain kind of perturbations, such as Bcl11b knockout and the treatment of Notch signaling pathway inhibitor GSI, in order to study the roles of these factors in T cell development.

2017-04-30 | GSE89198 | GEO

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

| PRJNA433410 | ENA

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16

| PRJNA475900 | ENA

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [RNA-seq]

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [RNA-seq]

| PRJNA434730 | ENA

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [ChIP-seq]

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [ChIP-seq]

| PRJNA475905 | ENA

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.

2021-05-12 | GSE155424 | GEO

ZBTB16 inhibits DNA replication and induces cell cycle arrest by targeting WDHD1 transcription in lung adenocarcinoma [RNA-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.

2024-04-24 | GSE263036 | GEO

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

2024-04-25 | GSE263037 | GEO