Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BBX regulates corticogenesis by repressing p53-mediated p21 expression.

ABSTRACT: This study aims to elucidate the role of BBX in embryonic neural stem cell maintenance. For mechanism study, we used mRNA sequencing to profile the transcriptional expression of E13.5 NSC upon BBX knockdown.

ORGANISM(S): Mus musculus

PROVIDER: GSE297615 | GEO | 2026/07/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

BBX regulates corticogenesis by repressing p53-mediated p21 expression. [set 2]

Project description:This study aims to elucidate the role of BBX in embryonic neural stem cell maintenance. For mechanism study, we used mRNA sequencing to profile the transcriptional expression of E13.5 NSC upon BBX knockdown and BBX+p21 co-knockdown.

2026-07-17 | GSE337091 | GEO

Rack1 is Essential for Corticogenesis by Preventing P21-Dependent Senescence in Neural Stem Cells

Project description:Normal neurodevelopment relies on intricate signaling pathways that balance neural stem cell (NSC) self-renewal, maturation and survival. Disruptions lead to neurodevelopmental disorders including microcephaly. Here, we implicate the inhibition of NSC senescence as a mechanism underlying neurogenesis and corticogenesis. We report that the receptor for activated C kinase (Rack1), a family member of WD40-repeat (WDR) proteins, is highly enriched in NSCs. Deletion of Rack1 in developing cortical progenitors leads to a microcephaly phenotype. Strikingly, the absence of Rack1 decreases neurogenesis and promotes a cellular senescence phenotype in NSCs. Mechanistically, the senescence-related p21 signaling pathway is dramatically activated in Rack1-null NSCs, and removal of p21 significantly rescues the Rack1-knockout phenotype in vivo. Finally, Rack1 directly interacts with Smad3 to suppress the activation of TGF-β/Smad signaling pathway, which plays a critical role in p21-mediated senescence. Our data implicate Rack1-driven inhibition of p21-induced NSC senescence as a critical mechanism behind normal cortical development.

2021-08-09 | PXD027798 |

TBR2 antagonizes retinoic acid dependent neuronal differentiation by repressing Zfp423 during corticogenesis.

Project description: Not available

| S-EPMC7032051 | biostudies-literature

Neural stem cells epigenomes and fate bias are temporally coordinated during corticogenesis [MPRA]

Project description:The cerebral cortex orchestrates complex cognitive functions, yet how its distinct temporal lineages are molecularly patterned during development remains unresolved. Here, we integrate single-cell transcriptomics and chromatin accessibility, together with genome-wide profiling of DNA methylation and 3D chromosomal contact across mouse corticogenesis (E13–E18) to elucidate cell fate transitions. We reveal using metacell flow analysis that neural stem cells (NSC) progressively shift from an intermediate progenitor–biased state toward an astrocytic lineage and that his process is accompanied with DNA methylation programming and chromosomal insulation changes. A model integrating transcription factor motif affinities with epigenetic features, identifies key regulators of cis-regulatory element (CRE) activation. In vivo reporter assays further decouple the intrinsic regulatory potential of CREs from context-dependent synergistic activation. Collectively, our findings uncover temporal epigenomic reprogramming that underlies the evolving differentiation potential of NSC, providing insights into the intrinsic and extrinsic mechanisms that pattern cortical lineages.

2026-06-10 | GSE292321 | GEO

Neural stem cells epigenomes and fate bias are temporally coordinated during corticogenesis [scATAC-seq]

2026-06-10 | GSE292319 | GEO

Neural stem cells epigenomes and fate bias are temporally coordinated during corticogenesis [scRNA-seq]

2026-06-10 | GSE292318 | GEO

Neural stem cells epigenomes and fate bias are temporally coordinated during corticogenesis [Methyl-Hi-C]

2026-06-10 | GSE292320 | GEO

To characterize the DMTF1 proximity proteome using BioID-mass spectrometry analysis

Project description:Neural stem cells (NSCs) contribute to brain development and homeostasis via their unique properties of self-renewal and differentiation. DMTF1 is a transcription factor that is proposed to be a tumor suppressor in cancer cells. However, the exact role of DMTF1 in NSC biology remains poorly understood. We found that DMTF1 depletion reduced the proliferation/self-renewal of mouse and human NSCs in vitro. To elucidate how DMTF1 may regulate gene transcription along with other proteins, we have employed BioID-mass spectrometry analysis of DMTF1 vs GFP proximity proteomes in 293T cells. The identified candidate DMTF1 protein interactors will subsequently be validated in mouse NSC. This study aims to investigate how DMTF1 regulates NSC proliferation.

2025-03-10 | PXD050501 | JPOST Repository

GDF11 slows excitatory neuronal senescence and brain ageing by repressing p21.

Project description: Not available

| S-EPMC10656444 | biostudies-literature

Cell cycle regulation: p53-p21-RB signaling.

Project description: Not available

| S-EPMC9090780 | biostudies-literature