Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

55 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SMAD3 ChIP-on-chip on A549 cell line

ABSTRACT: The aim of this study is to identify SMAD3 binding targets affected by the TGFb1/SMAD3 signal transduction on a genome-wide scale Formaldehyde cross-linked, sonicated chromatin was prepared from non-stimulated A549 cell line and stimulated with TGFb1. Chromatin immunoprecipated with anti-SMAD3 antibody is labeled with Cy5 and mock IP (with anti-FLAG antibody) is labeled with Cy3 and co-hybridized on Agilent Human Promoter Set arrays. Two biological replicates were performed.

ORGANISM(S): Homo sapiens

SUBMITTER: Kusum Pandit

PROVIDER: E-GEOD-28346 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

High throughput determination of TGFβ1/SMAD3 targets in A549 lung epithelial cells.

Zhang Yingze Y Handley Daniel D Kaplan Tommy T Yu Haiying H Bais Abha S AS Richards Thomas T Pandit Kusum V KV Zeng Qilu Q Benos Panayiotis V PV Friedman Nir N Eickelberg Oliver O Kaminski Naftali N

PloS one 20110520 5

<h4>Background</h4>Transforming growth factor beta 1 (TGFβ1) plays a major role in many lung diseases including lung cancer, pulmonary hypertension, and pulmonary fibrosis. TGFβ1 activates a signal transduction cascade that results in the transcriptional regulation of genes in the nucleus, primarily through the DNA-binding transcription factor SMAD3. The objective of this study is to identify genome-wide scale map of SMAD3 binding targets and the molecular pathways and networks affected by the T ...[more]

PMID: 21625455

Similar Datasets

ChIP-seq of mouse primary cultured bone marrow-derived neutrophils stimulated by lung cancer cell conditional medium

Project description:Bone marrow-derived neutrophils from C57BL/6J mice were treated with 10% LLC1 conditional medium or normal medium as the control for 2 hours, then processed using the SimpleChIP Enzymatic Chromatin IP Kit according to the manufacturer’s instructions. Antibodies against Smad3 and IgG isotype were used for immunoprecipitation. We performed ChIP-seq for Smad3 immuno-enriched DNA (Input and Smad3-IP) and mapped clean sequences against GRCm38 using Bowtie2, and peaks were identified using model-based analysis for ChIP-Seq (MACS) with default parameters.

2023-03-18 | E-MTAB-12740 | biostudies-arrayexpress

Smad3, Smad4 and TTF-1/NKX2-1 binding sites in H441/A549 lung cancer cell lines

Project description:We evaluated the role of TTF-1/NKX2-1 on Smad3 and Smad4 binding in lung cancer cell lines. Smad3 binding sites in A549 cells and Smad3, Smad4, and TTF-1/NKX2-1 binding sites in H441 cells were determined by ChIP-seq.

2014-07-27 | E-GEOD-51509 | biostudies-arrayexpress

RNAi profiling by array of of Smad2 and Smad3 in mouse mammary epithelial cells treated with TGF-beta to induce epithelial-to-mesenchymal transition

Project description:Effects of Smad3 and Smad2 knock-down on TGFbeta-induced epithelial-to-mesenchymal transition (EMT) in mouse mammary epithelial (Nme) cells

2009-04-01 | E-MEXP-1342 | biostudies-arrayexpress

Smad3 regulates the miR-200 family in gastric cancer

Project description:To find potential microRNA links between Smad3 and E-cadherin, we characterized the microRNA profiles of two gastric cancer cell lines: SNU484-LPCX, which does not express Smad3, and SNU484-Smad3, in which Smad3 is overexpressed. We found that miR-200 families, among other differentially expressed miRNAs, are overexpressed in SNU484-Smad3. Through subsequent studies, including silencing of Smad3 in SNU484-Smad3 and expression profiling of epithelial-mesenchymal markers and ZEB1/2, known repressors of E-cadherin, we found that Smad3 regulates miR-200 families at the transcriptional level, which regulate ZEB 1/2, known transcriptional repressors of E-cadherin, at the post-transcriptional level. This represents an important link between the TGF-beta signaling pathway and post-transcriptional regulation by miRNAs. Examination of small RNA expression in 2 different cell lines (SNU484-LPCX, SNU484-Smad3).

2011-09-14 | E-GEOD-27977 | biostudies-arrayexpress

Protection from obesity and diabetes by blockade of TGF-beta/Smad3 signaling

Project description:Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-beta/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3 deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3-/- white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3-/- adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-alpha1 expression. We observe significant correlation between TGF-beta1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-beta1 signaling protects mice from obesity, diabetes and hepatic steatosis. Together, these results demonstrate that TGF-beta signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-beta1 activity might be an effective treatment strategy for obesity and diabetes. Smad3-/- and WT mice were fed with regular diet (RD) and high fat diet (HFD), and diet induced obese (DIO) mice were treated with IgG and anti-TGF-b1 antibody

2011-07-12 | E-GEOD-28598 | biostudies-arrayexpress

The phosphorylation of the Smad2/3 linker region by Nemo-like kinase regulates TGF-β signaling

Project description:Smad2 and Smad3 (Smad2/3) primarily mediates the transforming growth factor-β (TGF-β) signaling that drives cell proliferation, differentiation, and migration. The dynamics of the Smad2/3 phosphorylation provides the key mechanism for regulating the TGF-β signaling pathway. Here we identified NLK as a novel regulator of TGF-β signaling pathway via modulating the phosphorylation of Smad2/3 in the linker region.

2021-09-10 | PXD023957 | Pride

SMAD3 ChIP-on-chip on A549 cell line

Project description:The aim of this study is to identify SMAD3 binding targets affected by the TGFb1/SMAD3 signal transduction on a genome-wide scale

2011-06-01 | GSE28346 | GEO

TGF-beta/Smad3-dependent gene expression analysis in naive CD4 T cells

Project description:Investigation of transcript level modulation in unstimulated and TGF-beta treated (with or without superimposed T-cell receptor and CD28 stimulation) naive CD4 T cells from wild type or Smad3-deficient littermate mice. Smad3 is a critical signaling molecule and transcription factor downstream of TGF-beta and mediates several of the TGF-beta dependent tolerogenic effects in T cells. This study was undertaken to unveil the transcriptionnal program controled by the TGF-b/Smad3 axis. Microarray study using RNA recovered after 6 hours of culture in either serum free media, serum-free media + TGF-beta (2.5ng/ml) or serum-free media + TGF-beta and anti-CD3e and anti-CD28 stimulation (3 conditions). Naive CD4 T cells (TCRb+, CD4+, CD62L+ and CD44-) were sorted from either wild type or Smad3 deficient littermates and submitted to the 3 culture conditions. Three biological replicates were obtained (each from at least 2 different mice). Thus a total of 18 Nimblegen 365K chip were used.

2012-08-31 | E-GEOD-40494 | biostudies-arrayexpress

Identification of genes associated with TGF-beta/Smad3-mediated renal inflammation and fibrosis by RNA sequencing

Project description:In this study, we employed high-throughput RNA sequencing (RNA-Seq) to identify the Smad3-dependent lncRNAs related to renal inflammation and fibrosis in Smad3 knockout (KO) mouse models of unilateral ureteral obstructive nephropathy (UUO) and immunologically-induced anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). 12 kidney tissue samples of Smad3 KO/WT mice from normal control, UUO at day 5 or anti-GBM GN at day 10 models (n=2 in each group) for whole transcriptome RNA-sequencing.

2014-03-26 | E-GEOD-55808 | biostudies-arrayexpress

Smad2 and Smad3 binding sites in H345-TbRII cells

Project description:Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta. Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).

2015-09-15 | E-GEOD-63871 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data