Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ep300 Cuttag for WT and DKO (Rara and Rxra deletion) of mESC RA-induced differentiation

ABSTRACT: To investigate the effect of Ep300 binding in Rara and Rxra deletion for mESC differetiation and development

ORGANISM(S): Mus musculus

PROVIDER: GSE315313 | GEO | 2026/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

microRNA-27a contributes to rhabdomyosarcoma cell proliferation through suppression of RARA and RXRA

Project description:microRNA-27a contributes to rhabdomyosarcoma cell proliferation through suppression of RARA and RXRA

| PRJNA229773 | ENA

microRNA-27a contributes to rhabdomyosarcoma cell proliferation through suppression of RARA and RXRA

Project description:This SuperSeries is composed of the SubSeries listed below. Background: Rhabdomyosarcomas (RMS) are rare but very aggressive tumors of childhood that arise as a consequence of regulatory distruption of the growth and differentiation pathways of myogenic precursor cells. Based on morphology, two major RMS subtypes can be identified: embryonal RMS (ERMS) and alveolar (ARMS). So, it is essential to unravel the molecular mechanisms involved in cancer pathogenesis and in disease progression. MicroRNAs are endogenous small non-coding RNAs with a key role in tumorigenesis. Methodology/Principal Findings: To better understand the involvement of miRNAs in RMS, we analyzed the expression profile of 8 different RMS cell lines (4 ARMS and 4 ERMS). The miRNA population from each cell line was compared to a reference sample consisting of a pool of each total RNA sample mixed in equal amount. We identified a 16 miRNAs signature that discriminates translocation positive (ARMS) and negative RMS (ERMS). We focused our attention on the role of miR-27a that is up-regulated in the more aggressive RMS cell lines (ARMS translocation positive) where probably it acts as an oncogene. miR-27a-overexpressing cells showed a significant enhance of the proliferation rate, paralleled by a decrease of cells in G1 phase. We demonstrated that miR-27a is implicated in cell cycle control by targeting the retinoic acid alpha receptor (RARA) and retinoic X receptor alpha (RXRA). Conclusions: Our results demonstrated the potential of miRNA expression signature to better classify different RMS subtypes and settled the basis for a potential therapeutic role of miR-27a in RMS through modulation of retinoic acid receptors expression.

2015-05-04 | GSE52679 | GEO

Lagonosticta rara

Project description:Lagonosticta rara

| PRJNA959989 | ENA

RarA Regulon

Project description:The experimental design was to determine the regulon of the transcriptional activator RarA. This was done by comparing the transcriptome profiles between a rarA overexpressor and the baseline control. RarA overexpression was achieved by plasmid mediated overexpression of the rarA gene and the baseline control was a vector only strain.

2013-03-21 | E-MEXP-3742 | biostudies-arrayexpress

Astrammina rara

Project description:Astrammina rara overview

| PRJNA47913 | ENA

Genome-wide analysis of RXRa binding in mouse liver chromatin with ChIP-SEQ.

Project description:For the genome-wide analysis using ChIP-Seq on mouse liver cells, a full accounting of all RXRÎ± binding sites and of RXRa related gene regulations is expected to address the main knowledge gap around RXRÎ±. Liver tissue of wild type and hs-RXRa-del-exon4-/- mice, male and female for each genotype have been ChIP-Seq'ed for RXRa and Pol2.

2014-04-01 | E-GEOD-21696 | biostudies-arrayexpress

Transcriptomic profiling of LLC LeptoM vector control, Nr1h2/3 DKO and RXRa/b/g TKO upon stimulation with 1μM 9 cis-retinoic acid (RA) in vitro

Project description:To understand transcriptional regulation of nuclear receptors, LXRs and RXRs, in leptomeningeal metastatic cancer cells, we use CRISPR-Cas9 to knockout Nr1h2/3 genes (encoding LXRβ/α) or RXRa/b/g genes (encoding RXRα/β/γ) in LLC LeptoM cell lines, with small guide RNA targeting lacZ as vector control. We then subjected these cell lines for bulk RNA sequencing with or without stimulation of 1μM 9 cis-RA. Pathway analysis of the differentially expressed genes between LLC LeptoM vector control with RA stimulation to DMSO treatment revealed upregulation of developmental related pathways and lipid metabolism pathways. Meanwhile, loss of function in LXR or RXR both resulted in dysregulation of multiple lipid metabolism pathways, in which RXR made a broader impact.

2024-10-13 | GSE277622 | GEO

RARA haploinsufficiency modestly influences the phenotype of APL.

Project description:RARA haploinsufficiency is an invariable consequence of t(15;17) reciprocal translocations in acute promyelocytic leukemia (APL). Furthermore, retinoids and RARA activity have been implicated in hematopoietic self-renewal, lineage commitment and neutrophil maturation. We and others therefore predicted that RARA haploinsufficiency would contribute to APL pathogenesis. To test this hypothesis we crossed RARA+/- mice with mice expressing PML-RARA from the Cathepsin G locus (mCG-PR). We found that RARA haploinsufficiency cooperated with PML-RARA, only modestly influencing the pre-leukemic and leukemic phenotype. Bone marrow from mCG-PR+/- x RARA+/- mice had decreased numbers of mature myeloid cells, increased ex vivo myeloid cell proliferation and an increased competitive advantage following transplantation. RARA haploinsufficiency did not alter mCG-PR dependent leukemic latency or penetrance, but did influence the distribution of leukemic cells; mCG-PR+/- x RARA+/- mice presented more commonly with low to normal white blood cell counts and with myeloid infiltration of lymph nodes. APL arising in these mice was responsive to ATRA, and had virtually no differences in expression profiling compared to tumors arising in mCG-PR+/- x RARA+/+ mice. These phenotypes were dependent on PML-RARA activity, since they were not detected in RARA+/- mice in the absence of the mCG-PR transgene. These data show that RARA haploinsufficiency (like PML haploinsufficiency and RARA-PML) can cooperate with PML-RARA to influence the pathogenesis and phenotype of APL in mice, but that PML-RARA is the driver of t(15;17) APL.

2010-07-29 | GSE23291 | GEO

Effect of PML/RARA on the transcriptome of preleukemic early promyelocytes vs PML/RARA-Flt3ITD leukemic promyelocytes

Project description:Transcriptional profiling of murine cells expressing PML/RARA at the early promyelocyte stage (4 weeks old, preleukemic) and in full blown PML/RARA leukemia generated by transducing PML/RARA bone marrow with a Flt3-ITD retroviral vector

2015-07-15 | GSE59431 | GEO

scRNA-seq for Klf5 or SE deletion of mESC differentiation

Project description:To investigate the effect of Klf5 or super enhancer deletion for mESC differetiation and development

2024-04-14 | GSE263578 | GEO