Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

ABSTRACT: To investigate the potential interactions between of Gata6 and Mib1 in OFT development, we generated a double heterozygous mice Mib1V943F/+ Gata6STOP/+, harvested OFT at E11.5, and determined gene expression profiles, using RNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE264238 | GEO | 2024/08/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:To investigate the role of Gata6 in OFT development, we generated a Gata6 heterozygous mice, harvested OFT at E11.5, and determined gene expression profiles, using bulk RNA-seq.

2024-08-26 | GSE255237 | GEO

Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

| PRJNA1101518 | ENA

Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

| PRJNA1074230 | ENA

ChIP-seq for Gata6 and histone H3K27Ac on mouse branchial arches at E11.5.

Project description:Gata6 ChIP-seq on mouse posterior branchial arches connected to outflow tract of the heart (PBA/OFT) at embryonic day (E) 11.5. H3K27Ac ChIP-seq on mouse second branchial arch (BA2) and posterior branchial arches connected to outflow tract of the heart (PBA/OFT) at embryonic day (E) 11.5.

2017-09-25 | E-MTAB-5407 | biostudies-arrayexpress

Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

2012-10-01 | GSE41179 | GEO

Characterisation of the outflow tract banded heart utilising RNA sequencing to direct functional analysis

Project description:Heart development is known to be influenced by haemodynamics, however the effects of abnormal load on gene expression are not clearly defined. To determine the hearts transcriptional response to stress, a model of haemodynamic alteration, outflow tract (OFT) banding, was employed in the chick embryo at HH21. Stereological and expression analysis were performed at HH29, with targeted expression studies at HH35. We defined a phenotype of left sided heart dilation and performed RNA sequencing on OFT-banded hearts compared to Sham controls. Globin transcripts were depleted in the RNA during library preparation, and 28 differentially expressed genes were identified. Expression appeared to represent a mechanism of cardioprotection with calcium sequestering, metabolic and developmental genes highlighted. Significant reductions in apoptosis were also seen. We have presented a model of left sided dilation in OFT-banded hearts and found differential expression of genes that may be associated with stress and maintaining cardiac output.

2020-03-16 | GSE120498 | GEO

Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

Project description:The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression. Refer to individual Series

2010-05-17 | E-GEOD-17936 | biostudies-arrayexpress

Gata4 regulates hedgehog signaling and Gata6 expression for outflow tract development.

Project description:Dominant mutations of Gata4, an essential cardiogenic transcription factor (TF), were known to cause outflow tract (OFT) defects in both human and mouse, but the underlying molecular mechanism was not clear. In this study, Gata4 haploinsufficiency in mice was found to result in OFT defects including double outlet right ventricle (DORV) and ventricular septum defects (VSDs). Gata4 was shown to be required for Hedgehog (Hh)-receiving progenitors within the second heart field (SHF) for normal OFT alignment. Restored cell proliferation in the SHF by knocking-down Pten failed to rescue OFT defects, suggesting that additional cell events under Gata4 regulation is important. SHF Hh-receiving cells failed to migrate properly into the proximal OFT cushion, which is associated with abnormal EMT and cell proliferation in Gata4 haploinsufficiency. The genetic interaction of Hh signaling and Gata4 is further demonstrated to be important for OFT development. Gata4 and Smo double heterozygotes displayed more severe OFT abnormalities including persistent truncus arteriosus (PTA). Restoration of Hedgehog signaling renormalized SHF cell proliferation and migration, and rescued OFT defects in Gata4 haploinsufficiency. In addition, there was enhanced Gata6 expression in the SHF of the Gata4 heterozygotes. The Gata4-responsive repressive sites were identified within 1kbp upstream of the transcription start site of Gata6 by both ChIP-qPCR and luciferase reporter assay. These results suggested a SHF regulatory network comprising of Gata4, Gata6 and Hh-signaling for OFT development.

| S-EPMC6550424 | biostudies-literature

Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

Project description:Neural crest defects lead to congenital heart disease involving outflow tract (OFT) malformation. Integrin-linked-Kinase (ILK) plays important roles in multiple cellular processes and embryogenesis. ILK is expressed in neural crest cells (NCC), but its role in NCC and OFT morphogenesis remains unknown. We used microarrays to detail the global programme of gene expression underlying the morphogenesis of the cardiac neural crest and outflow tract. The outflow tract of control and ILK mutant mouse embryos at E10.5 were dissected and dissociated. Neural crest cells were FACS sorted and used for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-01 | E-GEOD-41179 | biostudies-arrayexpress

Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

2010-05-17 | GSE17936 | GEO