Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

α1ACT is essential for survival and early cerebellar programming in a critical neonatal window [ChIP-Seq]

ABSTRACT: Previous study has shown that alpha1ACT is a transcription factor involved with regulating neuronal gene expression. We further performed ChIP-seq using pc12 cell lines stably expressing pcDNA3-alpha1ACT or control pcDNA3 vectors to identify genomic locus directly occupied by alpha1ACT

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE126088 | GEO | 2019/02/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

α1ACT is essential for survival and early cerebellar programming in a critical neonatal window [RNA-Seq]

Project description:Previous study has shown that alpha1ACT is a transcription factor involved with regulating neuronal gene expression. We performed a time-series RNA-seq study using pc12 cell lines stably expressing pcDNA3-alpha1ACT at 4 time points (6hr, 24hr, 3day, and 10day) to explore the transcriptional profiles that capture transient and prolonged dynamic changes regulated by alpha1ACT during cell cycle and differentiation

2019-02-06 | GSE126087 | GEO

?1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window.

Project description:Postnatal cerebellar development is a precisely regulated process involving well-orchestrated expression of neural genes. Neurological phenotypes associated with CACNA1A gene defects have been increasingly recognized, yet the molecular principles underlying this association remain elusive. By characterizing a dose-dependent CACNA1A gene deficiency mouse model, we discovered that ?1ACT, as a transcription factor and secondary protein of CACNA1A mRNA, drives dynamic gene expression networks within cerebellar Purkinje cells and is indispensable for neonatal survival. Perinatal loss of ?1ACT leads to motor dysfunction through disruption of neurogenesis and synaptic regulatory networks. However, its elimination in adulthood has minimal effect on the cerebellum. These findings shed light on the critical role of ?1ACT in facilitating neuronal development in both mice and humans and support a rationale for gene therapies for calcium-channel-associated cerebellar disorders. Finally, we show that bicistronic expression may be common to the voltage-gated calcium channel (VGCC) gene family and may help explain complex genetic syndromes.

| S-EPMC6533132 | biostudies-literature

α1ACT is essential for survival and early cerebellar programming in a critical neonatal window

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

2019-02-06 | GSE126089 | GEO

α1ACT is essential for survival and early cerebellar programming in a critical neonatal window

Project description:α1ACT is essential for survival and early cerebellar programming in a critical neonatal window

| PRJNA521000 | ENA

α1ACT is essential for survival and early cerebellar programming in a critical neonatal window [RNA-Seq]

Project description:α1ACT is essential for survival and early cerebellar programming in a critical neonatal window [RNA-Seq]

| PRJNA521003 | ENA

α1ACT is essential for survival and early cerebellar programming in a critical neonatal window [ChIP-Seq]

Project description:α1ACT is essential for survival and early cerebellar programming in a critical neonatal window [ChIP-Seq]

| PRJNA521004 | ENA

The target genes of transcript factor ZNF191

Project description:Transcriptional profiling of human embryo kidney cells comparing control HEK293 transfected with empty vectors cells with HEK293 cells transfected with pcDNA3-ZNF191 (or ZNF191 siRNA vector). We searched for early ZNF191 target genes by using a transient overexpression and knockdown strategy in the human embryo kidney (HEK293) cells. A table of gene targets of transcription factor ZNF191 commonly identified by both strategies is appended below as a supplementary file.

2009-12-31 | GSE14273 | GEO

MicroRNA expression profiling of NGF-treated PC12 cells revealed a critical role for miR-221 in neuronal differentiation

Project description:MicroRNAs (miRNAs) are small non-coding RNAs that control protein expression through translational inhibition or mRNA degradation. MiRNAs have been implicated in diverse biological processes such as development, proliferation, apoptosis and differentiation. Upon treatment with nerve growth factor (NGF), rat pheochromocytoma PC12 cells elicit neurite outgrowth and differentiae into neuron-like cells. NGF plays a critical role not only in neuronal differentiation but also in protection against apoptosis. In an attempt to identify NGF-regulated miRNAs in PC12 cells, we performed miRNAM-cM-^@M-^@microarray analysis using total RNAs harvested from cells treated with NGF. In response to NGF treatment, expression of 8 and 12 miRNAs were up- and down-regulated, respectively. Quantitative RT-PCR analysis confirmed increased expression of miR-221, miR-181a* and miR-326, and decreased expression of miR-143, miR-210 and miR-532-3p after NGF treatment, among which miR-221 was drastically up-regulated. Overexpression of miR-221 induced neurite outgrowth of PC12 cells in the absence of NGF treatment, and also enhanced neurite outgrowth caused by low-dose NGF. More importantly, knockdown of miR-221 by antagomir attenuated NGF-mediated neurite outgrowth. Finally, miR-221 decreased expression of Foxo3a and Apaf-1, both of which are involved in apoptosis in PC12 cells. Our results indicate that miR-221 plays a critical role for neuronal differentiation as well as protection against apoptosis in PC12 cells. NGF induced miRNAs expression in rat pheochromocytoma PC12 cells was measured in cells treated with 100 ng/ml NGF for 0, 12, 24 and 48 hr.

2012-05-15 | E-GEOD-32122 | biostudies-arrayexpress

MicroRNA expression profiling of NGF-treated PC12 cells revealed a critical role for miR-221 in neuronal differentiation

Project description:MicroRNAs (miRNAs) are small non-coding RNAs that control protein expression through translational inhibition or mRNA degradation. MiRNAs have been implicated in diverse biological processes such as development, proliferation, apoptosis and differentiation. Upon treatment with nerve growth factor (NGF), rat pheochromocytoma PC12 cells elicit neurite outgrowth and differentiae into neuron-like cells. NGF plays a critical role not only in neuronal differentiation but also in protection against apoptosis. In an attempt to identify NGF-regulated miRNAs in PC12 cells, we performed miRNA　microarray analysis using total RNAs harvested from cells treated with NGF. In response to NGF treatment, expression of 8 and 12 miRNAs were up- and down-regulated, respectively. Quantitative RT-PCR analysis confirmed increased expression of miR-221, miR-181a* and miR-326, and decreased expression of miR-143, miR-210 and miR-532-3p after NGF treatment, among which miR-221 was drastically up-regulated. Overexpression of miR-221 induced neurite outgrowth of PC12 cells in the absence of NGF treatment, and also enhanced neurite outgrowth caused by low-dose NGF. More importantly, knockdown of miR-221 by antagomir attenuated NGF-mediated neurite outgrowth. Finally, miR-221 decreased expression of Foxo3a and Apaf-1, both of which are involved in apoptosis in PC12 cells. Our results indicate that miR-221 plays a critical role for neuronal differentiation as well as protection against apoptosis in PC12 cells.

2012-05-16 | GSE32122 | GEO

Profiling gene expression in HeLa cells following TFEB transient transfection

Project description:Total RNA samples from three biological replicates in which TFEB was transiently overexpressed in HeLa cells by transfection using a pcDNA3 vector. As negative control, we used total RNA samples from HeLa cells transfected with an empty pcDNA3 vector.

2009-07-01 | GSE16267 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data