Gene expression in D4 WT and P38α KO uteri
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA820452 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18495983.fastq.gz | Fastqsanger.gz | |||
| SRR18495984.fastq.gz | Fastqsanger.gz | |||
| SRR18495985.fastq.gz | Fastqsanger.gz | |||
| SRR18495986.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Differential expression genes were normalized to fragments per kilobase of exon model per million mapped reads (RPKM) using EdgeR package in R with the criteria of fold change significantly greater than 2 or less than 0.5 and P<0.05.
2022-03-30 | GSE199500 | GEO
Project description:Gene expression in D8 WT and Menin KO uteri
| PRJNA756569 | ENA
Project description:p38α MAP kinase plays an important tumor suppressor role, which is mediated by both its negative effect on cell proliferation and its pro-apoptotic activity. Surprisingly, most tumor suppressor mechanisms coordinated by p38α have been reported to occur at the post- translational level. This contrasts with the important role of p38α in the regulation of transcription and the profound changes in gene expression that normally occur during tumorigenesis. We have analyzed whole genome expression profiles of Ras-transformed wild- type and p38α-deficient cells and have identified 202 genes that are potentially regulated by p38α in transformed cells. Expression analysis has confirmed the regulation of these genes by p38α in tumors, and functional validation has identified several of them as likely mediators of the tumor suppressor effect of p38α on Ras-induced transformation. Interestingly, about 10% of the genes that are negatively regulated by p38α in transformed cells contribute to EGF receptor signalling. Our results suggest that inhibition of EGF receptor signalling by transcriptional targets of p38α is an important function of this signalling pathway in the context of tumor suppression. We have investigated how transcriptional regulation contributes to the tumor suppressor effect of p38α, by comparing whole-genome expression profiles of wild-type (WT) and p38α- deficient (p38α-/-) mouse embryo fibroblasts (MEFs) expressing oncogenic H-RasG12V
2011-11-23 | E-GEOD-26762 | biostudies-arrayexpress
Project description:The P38α modulates proliferation, survival and differentiation of different kinds of celll. Here, we demonstrate that loss of P38α accelerates recovery from anemia in mice by promoting survival of erythroblasts. To identify gene expression changes in P38α+/- versus P38α-/- erythroblasts, we sorted erythroblasts from P38α+/- and P38α-/- mice during recovery from anemia and performed microarray analysis.
2018-12-21 | GSE111751 | GEO
Project description:ATACseq of WT and BRM KO cells at D4, D6 and D10 of cardiac differentiation
| PRJNA631414 | ENA
Project description:There is considerable evidence that inhibition of p38α mitogen-activated protein kinase diminishes cardiac damage during myocardial ischemia. During myocardial ischemia p38α interacts with TAB1, a scaffold protein, which promotes p38α autoactivation; active p38α (pp38α) then trans-phosphorylates TAB1. Previously, we solved the X-ray structure of the p38α-TAB1(384-412) complex. Here we further characterize the interaction by resolving the structure of the pp38α-TAB1(1-438) complex in the active state. Based on this information we created a global knock-in mouse with substitution of four residues on TAB1 (V390A, Y392A, V408G, M409A) we show are required for docking onto p38α. Whereas ablating p38α or TAB1 results in early embryonal lethality, the TAB1 KI mice are viable, develop normally and have no appreciable alteration in their lymphocyte repertoire or myocardial transcriptional profile. Nonetheless, following in vivo regional myocardial ischemia, infarction volume is significantly reduced and the trans- phosphorylation of TAB1 is disabled. Unexpectedly, the activation of myocardial p38α during ischemia is only mildly attenuated in TAB1 KI hearts, an effect most likely due to the removal of the steric hindrance to MAP2K3 binding. We conclude that it is the phosphorylation of TAB1 by pp38α during ischemia that is associated with cardiac damage. The data reveal that it is possible to selectively inhibit signalling downstream of p38α to attenuate ischemic injury. Our findings validate the p38α-TAB1 complex as a therapeutic target that may circumvent the toxicity associated with ATP-competitive inhibitors of p38α.
2018-08-27 | E-MTAB-6460 | biostudies-arrayexpress
Project description:To further study gene expression regulated by 17b-estradiol in uteri, we have employed whole gene microarray profiling to identify genes specifically regulated by this site of methylation of ERa (Arg260). Control littermates were used named WT.
2020-06-13 | GSE152344 | GEO
Project description:Single cell RNAseq of WT and BRG1 conditional KO at D4 and D10 of cardiac differentiation
| PRJNA631417 | ENA
Project description:Differentiation proceeds along a continuum of increasingly fate-restricted intermediates, referred to as canalization How robust canalization is established or maintained is unclear. Here we show that deletion of the BRG1/BRM-associated factor (BAF) chromatin remodeling complex ATPase gene Brm (encoding Brahma) results in a radical identity switch during directed cardiogenesis of mouse embryonic stem cells (ESCs). Despite establishment of well-differentiated precardiac mesoderm, Brm-null cells subsequently shifted identities, predominantly becoming neural precursors, violating germ layer assignment. Trajectory inference showed sudden acquisition of non-mesodermal identity in Brm-null cells, consistent with a new transition state inducing a saddle-node bifurcation. Mechanistically, loss of Brm prevented de novo accessibility of cardiac enhancers while increasing expression of the neurogenic factor POU3F1 and preventing expression of the neural suppressor REST. Brm mutant identity switch was overcome by increasing BMP4 levels during mesoderm induction, repressing Pou3f1 and re-establishing a cardiogenic chromatin landscape. Our results reveal BRM as a compensable safeguard for fidelity of mesoderm chromatin states, and support a model in which developmental canalization is not a rigid irreversible path, but a highly plastic trajectory that must be safeguarded. We invetigated H3K27ac and H3K27me3 marks in WT and BRM KO cells at D4 and D10 stages of cardiac differentiation
2021-10-27 | GSE150182 | GEO