ChIPseq Smad3-JMJD3
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Project description:ChIP seq of endogenous Smad3 and JMJD3 proteins in mouse embryonic neural stem cells treated with TGFbeta during 30 minutes. Neural stem cells were treated with TGFbeta during 30 minutes, and then chromatin immunoprecipitation was carried out with specific JMJD3 or Smad3 antibodies. Positive and negative controls for each immunoprecipitation were checked before sequencing. Input was used to normalized the sequencing results.
2011-12-30 | E-MTAB-825 | biostudies-arrayexpress
Project description:Neural development requires crosstalk between signaling pathways and chromatin. In this study, we demonstrate that neurogenesis is promoted by an interplay between the TGFM-NM-2 pathway and the H3K27me3 histone demethylase (HDM) JMJD3. Genome-wide analysis showed that JMJD3 is targeted to gene promoters by Smad3 in neural stem cells (NSCs) and is essential to activate TGFM-NM-2-responsive genes. In vivo experiments in chick spinal cord revealed that the generation of neurons promoted by Smad3 is dependent on JMJD3 HDM activity. Overall, these findings indicate that JMJD3 function is required for the TGFM-NM-2 developmental program to proceed. We immunoprecipitate endogenous Smad3 or JMJD3 proteins from neural stem cells treated with TGFb for 30 minutes.
2012-05-30 | E-GEOD-36673 | biostudies-arrayexpress
Project description:Neural development requires crosstalk between signaling pathways and chromatin. In this study, we demonstrate that neurogenesis is promoted by an interplay between the TGFβ pathway and the H3K27me3 histone demethylase (HDM) JMJD3. Genome-wide analysis showed that JMJD3 is targeted to gene promoters by Smad3 in neural stem cells (NSCs) and is essential to activate TGFβ-responsive genes. In vivo experiments in chick spinal cord revealed that the generation of neurons promoted by Smad3 is dependent on JMJD3 HDM activity. Overall, these findings indicate that JMJD3 function is required for the TGFβ developmental program to proceed.
2012-05-30 | GSE36673 | GEO
Project description:Several signaling pathways require JMJD3 binding to promoters to activate the expression of target genes. Despite the known H3K27me3 demethylase activity of JMJD3 the transcriptional coactivator mechanism remains unclear. Here we reveal that JMJD3 promotes transcription of TGFb responsive genes through regulation of RNAPII progression on gene bodies. ChIPseq experiments demonstrate that upon TGFb treatment, JMJD3 and RNAPII.ser2P colocalyze extensively along intragenic regions of TGF target genes. M-BM- According to these data, genome wide analysis shows that JMJD3 dependent TGF target genes are enriched in H3K27me3 prior to TGF signaling pathway activation. M-BM- Further molecular analysis indicate that JMJD3 removes H3K27me3 and pave the way for the RNAPII.Overall, these findingsM-BM- uncover the mechanism ofM-BM- JMJD3 function in transcriptional activation We performed chromatin immunoprecipitation followed by sequencing (ChIPseq) of H3K27me3 mark in mouse neural stem cells growing under standard conditions. We also performed ChIPseq of elongating RNAPII (Ser2P) and JMJD3 in neural stem cells stimulated with TGFb cytokine.
2012-12-31 | E-GEOD-38269 | biostudies-arrayexpress
Project description:Neural development requires crosstalk between signaling pathways and chromatin. In this study, we demonstrate that neurogenesis is promoted by an interplay between the TGFM-NM-2 pathway and the H3K27me3 histone demethylase (HDM) JMJD3. Genome-wide analysis showed that JMJD3 is targeted to gene promoters by Smad3 in neural stem cells (NSCs) and is essential to activate TGFM-NM-2-responsive genes. In vivo experiments in chick spinal cord revealed that the generation of neurons promoted by Smad3 is dependent on JMJD3 HDM activity. Overall, these findings indicate that JMJD3 function is required for the TGFM-NM-2 developmental program to proceed Mouse neural stem cells (NSC) control and JMJD3 knock down (shctrl and shJMJD3) were treated with the vehicle (-TGFb) or TGFbeta 5ng/ml (+TGFb) for 2.5h. Three replicates were performed for each point. And all of them were use it to posterior analysis.
2012-04-30 | E-GEOD-35361 | biostudies-arrayexpress
Project description:Neural development requires crosstalk between signaling pathways and chromatin. In this study, we demonstrate that neurogenesis is promoted by an interplay between the TGFβ pathway and the H3K27me3 histone demethylase (HDM) JMJD3. Genome-wide analysis showed that JMJD3 is targeted to gene promoters by Smad3 in neural stem cells (NSCs) and is essential to activate TGFβ-responsive genes. In vivo experiments in chick spinal cord revealed that the generation of neurons promoted by Smad3 is dependent on JMJD3 HDM activity. Overall, these findings indicate that JMJD3 function is required for the TGFβ developmental program to proceed
2012-05-01 | GSE35361 | GEO
Project description:Several signaling pathways require JMJD3 binding to promoters to activate the expression of target genes. Despite the known H3K27me3 demethylase activity of JMJD3 the transcriptional coactivator mechanism remains unclear. Here we reveal that JMJD3 promotes transcription of TGFb responsive genes through regulation of RNAPII progression on gene bodies. ChIPseq experiments demonstrate that upon TGFb treatment, JMJD3 and RNAPII.ser2P colocalyze extensively along intragenic regions of TGF target genes. According to these data, genome wide analysis shows that JMJD3 dependent TGF target genes are enriched in H3K27me3 prior to TGF signaling pathway activation. Further molecular analysis indicate that JMJD3 removes H3K27me3 and pave the way for the RNAPII.Overall, these findings uncover the mechanism of JMJD3 function in transcriptional activation
2012-12-31 | GSE38269 | GEO
Project description:Smad2, Smad3, Smad4 and Foxh1 ChIPseq performed in pluripotent mESC and embryonic bodies (EBs). RNAseq were performed in WT mESCs and Ebs of WT, Smad2KO, Smad3KO and Smad2/3DKO.
2019-09-05 | GSE125116 | GEO
Project description:Although numerous genetic loci have been associated with coronary artery disease (CAD) with genome wide association studies (GWAS), efforts are needed to identify the causal genes in these loci and link them into fundamental signaling pathways. Toward that end, experiments reported here extend our investigation of the disease mechanism of CAD associated gene SMAD3, a central transcriptional intermediate in the TGFb pathway, investigating its role in smooth muscle biology. In vitro studies in human coronary artery smooth muscle cells (HCASMC) revealed that SMAD3 modulates cell state decisions in this cell type, promoting expression of differentiation marker genes and migration while inhibiting proliferation. RNA and chromatin immunoprecipitation sequencing (ChIPseq) studies in HCASMC identified downstream genes that reside in pathways which mediate vascular development and disease processes, including those related to atherosclerosis pathophysiology, expanding understanding of the TGFb canonical pathway in this cell type. ChIPseq studies also found colocalization of SMAD3 binding in loci targeted by TCF21, a CAD associated transcription factor that has been shown to produce a CAD protective de-differentiation program in HCASMC. In loci where these factors are juxtaposed on DNA, SMAD3 binding was anti-correlated with TCF21, and increased in cells depleted of TCF21, as shown by ChIPseq and ChIP experiments. Further, reporter gene studies revealed that while SMAD3 increased transcription at a SERPINE1 enhancer, and this effect was blocked by TCF21. Together, these data suggest that SMAD3 regulation of gene expression is modulated by TCF21, through independent regulation of jointly occupied genes and through epigenetic and possibly direct protein-protein interactions. Finally, eQTL studies in HCASMC indicated that SMAD3 expression is directly associated with increased disease risk, opposing the known protective effect of TCF21. We propose that the pro-differentiation function of SMAD3 inhibits HCASMC dedifferentiation of these cells as they respond to vascular stresses and expand and migrate to stabilize the plaque, and that SMAD3 function is directly opposed at the transcriptional level by the disease protective expression of TCF21, which promotes dedifferentiation and phenotypic modulation.
2018-09-11 | GSE115317 | GEO
Project description:Autophagy is essential for cellular survival and energy homeostasis under nutrient deprivation. Despite the emerging importance of nuclear events in autophagy regulation, epigenetic control of autophagy gene transcription remains unclear. Here, we identify Jumonji-D3 (JMJD3/KDM6B) histone demethylase as a key epigenetic activator of hepatic autophagy. Upon fasting-induced fibroblast growth factor-21 (FGF21) signaling, JMJD3 epigenetically upregulated global autophagy-network genes, including Tfeb, Atg7, Atgl, and Fgf21, through demethylation of histone H3K27-me3, resulting in autophagy-mediated lipid degradation. Mechanistically, phosphorylation of JMJD3 at Thr-1044 by FGF21 signal-activated PKA increased its nuclear localization and interaction with the nuclear receptor PPARto transcriptionally activate autophagy. Chronic administration of FGF21 in obese mice improved defective autophagy and hepatosteatosis in a JMJD3-dependent manner. Remarkably, in non-alcoholic fatty liver disease patients, hepatic expression of JMJD3, ATG7, LC3, and KL were substantially decreased. These findings demonstrate that FGF21-JMJD3 signaling epigenetically links nutrient deprivation with hepatic autophagy and lipid degradation in mammals
2020-05-26 | PXD015672 | Pride