Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide distribution of histone modification H3K36me3 in ECs during VEGF-signaling

ABSTRACT: Genome-wide distribution of histone modification H3K36me3 in ECs during VEGF-signaling

PROVIDER: PRJNA805229 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17973906.fastq.gz	Fastqsanger.gz
	SRR17973907.fastq.gz	Fastqsanger.gz
	SRR17973908.fastq.gz	Fastqsanger.gz
	SRR17973909.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Genome-wide distribution of histone modification H3K36me3 in ECs during VEGF-signaling

Project description:Vascular endothelial growth factor (VEGF) signaling serves a central role in vascular development as well as maintaining vascular homeostasis. In endothelial cells (ECs), VEGF activates gene expression of angiogenic transcription factors (TFs) followed by downstream induction of angiogenic responsive genes. Recent findings support histone modification dynamics contribute to transcriptional control of genes important for EC functions. Lysine demethylase 2B (KDM2B) demethylates histone H3K4me3 and H3K36me2/3 and also mediates monoubiquitylation of histone H2A119K. KDM2B functions as a transcriptional repressor in somatic cell reprograming and tumor development. However, the role of KDM2B during VEGF-signaling remains to be elucidated. Here, we show in cultured human ECs that knockdown of KDM2B enhances VEGF-induced angiogenesis via increased abilities of migration and proliferation. In contrast, ectopic expression of KDM2B has inhibitory effects on angiogenesis. The function of KDM2B is possibly dependent on its catalytic Jumondi C domain. Genome-wide analysis further reveal that KDM2B selectively controls transcription of VEGF-induced angiogenic TFs where increased H3K4me3/H3K36me3 and decreased of H2A119Kub are associated. These findings suggest an essential role of KDM2B during VEGF-signaling in ECs. Because dysregulation of VEGF signaling in ECs is involved in various diseases including cancer, KDM2B may be a potential therapeutic target in VEGF-mediated vasculopathic diseases.

2022-04-01 | GSE196503 | GEO

RNA-seq analysis to examine the effect of KDM2B knockdown or overexpression on transcriptional responses in ECs during VEGF-signaling

2022-04-01 | GSE196505 | GEO

Transcriptome and epigenetic characterization of ECs during VEGF-signaling

Project description:Transcriptome and epigenetic characterization of ECs during VEGF-signaling

| PRJNA805221 | ENA

Gene expression profiling of endothelial cells derived from Foxo1(+/+) and Foxo1(-/-) ES cells in response to VEGF

Project description:VEGF induces elongation of endothelial cells (ECs) that are derived from wild-type (Foxo1(+/+)) ES cells. VEGF-induced EC elongation is an important process of angiogenesis. ECs derived from Foxo1(-/-) ES cells fail to elongate in response to VEGF. Gene expression profiling of wild-type and Foxo1(-/-) ECs in the presence or absence of VEGF stimulation identifies responsible genes that regulate EC elongation. One wild-type (Foxo1(+/+)) ES cell clone and one Foxo1(-/-) ES cell clone were used. ES cells were cultured on OP9 stromal cell layer in the presence or absence of VEGF (10 ng/ml). After 6.5 days, VE-cadherin+ CD31+ ECs were isolated by FACS and used for total RNA extraction. Three independent experiments were performed for each condition.

2016-02-16 | E-GEOD-76366 | biostudies-arrayexpress

Gene expression profiling of endothelial cells derived from Foxo1(+/+) and Foxo1(-/-) ES cells in response to VEGF

2016-02-16 | GSE76366 | GEO

Histone modification profiles on Human Umbilical Vein Endothelial Cells (HUVECs) under Vasucular Endothelial Cell Growth Factor (VEGF) stimulation

Project description:Endothelial cells (ECs) are phenotypically heterogeneous mainly due to their dynamic epigenetic status. VEGF, the best-known angiogenic factor, activates calcium-NFAT signalling following acute angiogenic gene transcription. Here, we evaluated the global mapping of VEGF-mediated dynamic transcriptional events with a particular focus on major histone-code profiles using ChIP-seq. Remarkably, the regulatory regions of angiogenic transcription factors exclusively acquired embryonic stem-like bivalent histone marks after the VEGF stimulus. Moreover, the newly discovered NFAT-associated epigenome modifier, PTIP in the COMPASS complex, directed gene transcription via MLL3/4-enrichment which overwhelmed the polycomb-brakes. The non-canonical polycomb1 variant, PRC1.3, specifically bound to and allowed the transactivation of PRC2-enriched bivalent angiogenic genes until conventional PRC1 association and gene silencing. Knockdown of these epigenome modifiers abrogated postnatal aberrant neovessel formation via selective inhibition of acute angiogenic bivalent gene transcription. Collectively, the reported dynamic epigenome landscape in ECs may support the development of advanced therapeutic strategies against various vasculopathies.

2021-10-06 | GSE159075 | GEO

Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

Project description:Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

| PRJNA433476 | ENA

RNA-seq of human umbilical vein endothelial cells (HUVECs) stimulated with recombinant Vascular Endothelial Growth Factor A (VEGF-A) against untreated control

Project description:In order to identify new genes potentially involved in angiogenesis process, we performed a deep-sequencing transcriptome analysis of HUVECs stimulated with recombinant VEGF-A, introducing a difference with respect to the several previous studies. Primary ECs are normally cultured in vitro using an endothelial growth medium (EGM) constituted by an endothelial basal medium (EBM) supplemented with 2% fetal bovine serum (FBS) and a mix of growth factors and reagents, typically represented by basic Fibroblast Growth Factor (bFGF), Insulin-like Growth Factor 1 (IGF1), Epidermal Growth Factor (EGF), heparin, hydrocortisone, ascorbic acid and the same VEGF-A. In previous studies, HUVECs or other primary ECs were starved in EBM with low FBS concentration before the stimulation with VEGF-A. Instead of starvation, we grown HUVECs in complete EGM-2 medium except for VEGF-A to maintain the best condition for in vitro survival and propagation of primary ECs. After 24 hours of VEGF-A deprivation, VEGF-A was re-added to the medium and the stimulation was performed for six hours.

2021-04-08 | E-MTAB-9337 | biostudies-arrayexpress

Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

Project description:Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

| PRJNA593576 | ENA

Transcripts with H3K36me3 modification at differente stages of pancreas organogensis [CUT&Tag]

Project description:Transcripts with H3K36me3 modification at differente stages of pancreas organogensis [CUT&Tag]

| PRJNA905379 | ENA