Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation

ABSTRACT: Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation

PROVIDER: PRJNA1095834 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28538700_1.fastq.gz	Fastqsanger.gz
	SRR28538700_2.fastq.gz	Fastqsanger.gz
	SRR28538701_1.fastq.gz	Fastqsanger.gz
	SRR28538701_2.fastq.gz	Fastqsanger.gz
	SRR28538702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 148

Similar Datasets

Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation

Project description:Retinoic acid (RA), the major active metabolite of vitamin A, is essential for organogenesis, homeostasis, and tissue morphogenesis. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. To analyze the function of RA signaling during perinatal heart development, we investigated the mRNA expression levels of multiple retinoid metabolic genes at various perinatal stages using RNA-seq analysis.

2024-08-13 | GSE263095 | GEO

Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

Project description:Retinoic acid (RA), the major active metabolite of vitamin A, is essential for organogenesis, homeostasis, and tissue morphogenesis. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. For a comprehensive transcriptional evaluation of the effect of RA signaling on neonatal cardiomyocyte cell cycle arrest and maturation, we performed RNA-seq analysis of cultured perinatal cardiomyocytes treated with all-trans retinoic acid (ATRA) in vitro.

2024-08-13 | GSE263096 | GEO

Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

Project description:Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

| PRJNA1095836 | ENA

Phosphoproteome of RA-responsive and RA-resistant breast cancer cell lines

Project description:Retinoic acid (RA), the main active vitamin A metabolite, controls multiple biological processes such as cell proliferation and differentiation through genomic programs and kinase cascades activation. Due to these properties, RA has proven anti-cancer capacity. Several breast cancer cells respond to the antiproliferative effects of RA, while others are RA-resistant. However, the overall signaling and transcriptional pathways that are altered in such cells have not been elucidated. Here, in a large-scale analysis of the phosphoproteins and in a genome-wide analysis of the RA-regulated genes, we compared two human breast cancer cell lines, a RA-responsive one, the MCF7 cell line, and a RA-resistant one, the BT474 cell line, which depicts several alterations of the "kinome".

2016-07-05 | PXD004357 | Pride

Phosphoproteome of RA-responsive and RA-resistant breast cancer cell lines

2020-10-15 | PXD005911 | Pride

Meningeal-derived retinoic acid regulates neurogenesis via suppression of Notch and Sox2 [CUT&Run]

Project description:During development, the meninges act as a regulator of neocortical development by secreting ligands that act on neural cells to regulate neurogenesis and neuronal migration. Meninges-derived retinoic acid (RA) promotes neocortical progenitor cell cycle exit however the underlying mechanism is unknown. Here, we use Foxc1-mutant embryos that lack meninges-derived ligands, spatial transcriptomics, and profiling of retinoic-acid receptor-a (RARa) DNA binding to identify the neurogenic transcriptional mechanisms of RA signaling in cortical neural progenitors. We determined that meningeal-derived RA controls neurogenesis by suppressing self-renewal pathways Notch signaling and the transcription factor Sox2. We show that RARα binds in the Sox2ot promoter, a long non-coding RNA that regulates Sox2 expression, and RA promotes Sox2ot expression in neocortical progenitors. Our findings elucidate a previously unknown mechanism of howmeningeal RA coordinates neocortical development and insight into how defects in meningeal develop can cause neurodevelopmental disorders.

2024-09-25 | GSE269282 | GEO

Meningeal-derived retinoic acid regulates neurogenesis via suppression of Notch and Sox2 [Spatial Transcriptomics]

2024-09-25 | GSE269283 | GEO

Murine embryonic stem cells synthesize retinoic acid to promote their own spontaneous differentiation

Project description:Embryonic stem cells (ESC) are derived from blastocyst-stage embryos and are thought to be functionally equivalent to the inner cell mass in their developmental potential. ESCs pluripotency is maintained through a complex interplay of different signaling pathways and a network of transcription factors, which is centered around Oct3/4, Sox2 and Nanog. Although, in general, much is known about this pluripotency self-renewal circuitry, the molecular events that lead ESC to exit from pluripotency and begin differentiation are currently less known. Retinoic acid, an active metabolite of the vitamin A (retinol), plays important and pleiotropic roles in vertebrate embryonic development and ESC differentiation. Here we demonstrate that RA promotes early steps of ESC differentiation, and that ESC increase their capacity to synthesize RA during spontaneous differentiation as embryoid bodies, up-regulating the RA biosynthetic pathway components RDH1, RDH10, ADH3, RALDH2, and CRABP2. Microarray derived from total RNA of mESC not treated or treated with all-trans retinoic acid (ATRA) for 2 hours.

2016-02-10 | E-GEOD-66043 | biostudies-arrayexpress

Inhibition of 13-cis retinoic acid-induced gene expression of reactive-resistance genes by thalidomide in glioblastoma tumours in vivo

Project description:The cell differentiation potential of 13-cis retinoic acid (RA) has not succeeded in the clinical treatment of glioblastoma (GBM) so far. However, RA may also induce the expression of disistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL). Therefore, we tested if combined treatment with RA+THAL may inhibit growth of glioblastoma in vivo. Treatment with RA+THAL but not RA or THAL alone significantly inhibited tumour growth. The synergistic effect of RA and THAL was corroborated by the effect on proliferation of glioblastoma cell lines in vitro. HOXB7 was not upregulated but microarray analysis validated by real-time PCR identified four potential resistance genes (IL-8, HILDPA, IGFBPA, and ANGPTL4) whose upregulation by RA was suppressed by THAL. Furthermore, genes coding for small nucleolar RNAs (snoRNA) were identified as a target for RA for the first time, and their upregulation was maintained after combined treatment. Pathway analysis showed upregulation of the Ribosome pathway and downregulation of pathways associated with proliferation and inflammation. Combined treatment with RA + THAL delayed growth of GBM xenografts and suppressed putative resistance genes associated with hypoxia and angiogenesis. This encourages further pre-clinical and clinical studies of this drug combination in GBM. The purpose was to study differential gene expression in glioblastoma xenografts after treatment with 13-cis retinoic acid (RA), thalidomide (Thal) or a combination of both drugs.

2015-07-23 | E-GEOD-71224 | biostudies-arrayexpress

Gene regulation by phosphomimetic Myc and retinoic acid

Project description:We aimed to investigate the E-box and Max-independent functions of the oncogene Myc in gene regulation and differentiation of leukemic cells. Expression in HL60 leukemic cells of a mutant form of Myc with impaired Max and E-box interaction by replacing the phosphorylation sites of Pak2 kinase to aspartic acid (MycD), resulted in downregulation of 235 genes and, interestingly, upregulation of 586 genes. Eleven percent of the genes upregulated by MycD coincided with those stimulated by a short treatment of retinoic acid (RA) alone. When leukemic cells expressing MycD were stimulated with RA, the overlap with the RA-alone signature increased to 32% (492/1556 genes). Importantly, 320 of these 492 bona-fide direct RA target genes were specifically superactivated in presence of MycD (MycD+RA>RA), and not by MycA (MycD+RA>MycA+RA), further suggesting a synergy between the two pathways. The list of superactivated genes included important regulators of development and differentiation such as GATA6, ICAM1 and HOX genes, whose expression was validated in independent experiments by RT-qPCR. Induced gene expression in HL60 cells was measured after a short-treatment of retinoic acid (100nM, 4 hours). Cells were either wild-type or expressing ER-tagged MycD or MycA. Four biologically independent experiments were performed at each time.

2012-01-05 | E-GEOD-24731 | biostudies-arrayexpress

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