Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]

ABSTRACT: Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]

PROVIDER: PRJNA549710 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9328944.fastq.gz	Fastqsanger.gz
	SRR9328945.fastq.gz	Fastqsanger.gz
	SRR9328946.fastq.gz	Fastqsanger.gz
	SRR9328947.fastq.gz	Fastqsanger.gz
	SRR9328948.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Bcl6 binding sites and neurogenic activity in in vitro cortical progenitors

Project description:Bcl6 binding sites and neurogenic activity in in vitro cortical progenitors

| PRJNA549714 | ENA

Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]

Project description:Chromatin immunoprecipitation following Bcl6 induction (24h doxycycline) in mouse ES-cell-derived cortical progenitors (differentiation day 12).

2019-06-20 | GSE132964 | GEO

Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]

Project description:Transcriptome analysis following Bcl6 induction (24h doxycycline) in mouse ES-cell-derived cortical progenitors (differentiation day 12) shows that Bcl6 promotes a neurogenic transcription program and represses selective genes of the main proliferative pathways.

2019-06-20 | GSE133031 | GEO

Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]

Project description:Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]

| PRJNA549718 | ENA

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway II

Project description:Developmental neuron death plays a pivotal role in refining organization and wiring during neocortex formation. Aberrant regulation of this process results in neurodevelopmental disorders including impaired learning and memory. Underlying molecular pathways are incompletely determined. Loss of Bcl11a in cortical projection neurons induces pronounced cell death in upper-layer cortical projection neurons during postnatal corticogenesis. We used this genetic model to explore genetic mechanisms by which developmental neuron death is controlled. Unexpectedly, we found Bcl6, previously shown to be involved in transition of cortical neurons from progenitor to postmitotic differentiation state to provide a major check point regulating neuron survival during late cortical development. We show that Bcl11a is a direct transcriptional regulator of Bcl6. Deletion of Bcl6 exerts death of cortical projection neurons. In turn, reintroduction of Bcl6 into Bcl11a mutants prevents induction of cell death in these neurons. Together, our data identify a novel Bcl11a/Bcl6-dependent molecular pathway in regulation of developmental cell death during corticogenesis.

2022-06-24 | GSE185288 | GEO

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway I

2022-06-24 | GSE185287 | GEO

Bcl6 binding sites and neurogenic activity in in vitro cortical progenitors

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

2019-06-20 | GSE133032 | GEO

Phosphoproteome of fibro/adipogenic progenitors treated by Musclin in vitro

Project description:Fibro/adipogenic progenitors were isolated and treated by Musclin for 48 hours in vitro.

2021-09-14 | PXD028468 |

Fezf2 overexpression in murine cortical progenitors in vivo

Project description:Corticospinal motor neurons (CSMN) are one specialized class of cortical excitatory neurons, which connect layer Vb of the cortex to the spinal cord. a master transcription factor –Forebrain expressed zinc finger 2 (Fezf2) – has been identified that is necessary for the fate specification of CSMN. Fezf2 alone can cell-autonomously instruct the acquisition of CSMN-specific features when expressed in diverse, permissive cellular contexts, in vivo. In order to understand the molecular logic underlying the acquisition of CSMN traits upon Fezf2 expression, we compared the in vivo gene expression of FACS-purified cortical progenitors that ectopically expressed Fezf2 to control progenitors. We used in utero electroporation to deliver Fezf2GFP or CtrlGFP expression vectors to neocortical progenitors at E14.5, when they primarily generate CPN of the upper layers. Overexpression of Fezf2 in these progenitors is sufficient to instruct a fate-switch resulting in the generation of CSMN and other subtypes of corticofugal projection neurons. Fezf2GFP- and CtrlGFP -electroporated progenitors were FACS-purified at 24 and 48 hours after surgery and acutely profiled by microarrays.

2014-07-06 | E-GEOD-56451 | biostudies-arrayexpress

Apical progenitors remain multipotent throughout cortical neurogenesis

Project description:Apical progenitors remain multipotent throughout cortical neurogenesis

| PRJNA505836 | ENA