Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

5 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse NFI-C knock out embryonic fibroblasts

ABSTRACT: The Nuclear Factor I C (NFI-C) transcription factor has been implicated in TGF-Î² signaling, extracellular matrix deposition and skin appendage pathologies. We performed a global gene expression analysis in NFI-C-/- and wild-type embryonic primary murine fibroblasts. This indicated that NFI-C acts mostly to repress gene expression in response to TGF-Î²1. Misregulated genes featured a prominent over-representation of regulators of connective tissue inflammation and repair. Experiment Overall Design: mRNAs were isolated from embryonic fibroblasts obtained from 3 wild-type and 3 NFI-C knock-out mice, and their levels were probed using microarrays. Prior to RNA extraction, fibroblast cultures were treated or not with TGF-Î²1 for 1 hour to examine the immediate response to the growth factor, or treated for 10 hours to assess the delayed response.

ORGANISM(S): Mus musculus

SUBMITTER: Milos Pjanic

PROVIDER: E-GEOD-15871 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Nuclear factor I-C links platelet-derived growth factor and transforming growth factor beta1 signaling to skin wound healing progression.

Plasari Genta G Calabrese Alessandra A Dusserre Yves Y Gronostajski Richard M RM McNair Alan A Michalik Liliane L Mermod Nicolas N

Molecular and cellular biology 20090914 22

Transforming growth factor beta (TGF-beta) and platelet-derived growth factor A (PDGFAlpha) play a central role in tissue morphogenesis and repair, but their interplay remain poorly understood. The nuclear factor I C (NFI-C) transcription factor has been implicated in TGF-beta signaling, extracellular matrix deposition, and skin appendage pathologies, but a potential role in skin morphogenesis or healing had not been assessed. To evaluate this possibility, we performed a global gene expression a ...[more]

PMID: 19752192

Similar Datasets

Expression data from NFI-C knock out embryonic fibroblasts

Project description:The Nuclear Factor I C (NFI-C) transcription factor has been implicated in TGF-β signaling, extracellular matrix deposition and skin appendage pathologies. We performed a global gene expression analysis in NFI-C-/- and wild-type embryonic primary murine fibroblasts. This indicated that NFI-C acts mostly to repress gene expression in response to TGF-β1. Misregulated genes featured a prominent over-representation of regulators of connective tissue inflammation and repair.

2009-11-05 | GSE15871 | GEO

Genome-wide mapping of Nuclear Factor I binding sites using ChIP-Seq in WT and NFI-C knock-out MEFs

Project description:The Nuclear Factor I (NFI) family of DNA binding proteins (also called CAAT box transcription factors or CTF) is involved both in replication of adenoviral DNA and in regulation of gene expression. Using chromatin immuno-precipitation and high throughput sequencing (method termed ChIP-Seq) we performed genome-wide mapping of Nuclear Factor I DNA binding sites in mouse embryonic fibroblasts. We found that in vivo and in vitro NFI binding specificities are identical, since previously established position weight matrix was found to accurately predict binding sites for NFI group of proteins. Positional correlation between + and - strand ChIP-Seq tags revealed that NFI is a nucleosome-binding protein, unlike some other transcription factors. We further found that NFI binding correlates with the specific histone modification H3K4me3, the marker of transcribed promoters. Combining ChIP-Seq with the microarray expression data, we found that NFI associates with promoters with higher transcription level. We estimate that transcribed promoters may be more accessible to transcription factor binding than their nearby regions since NFI preferentially bind their DNA target sites located around transcription start sites. Knocking-out one of the NFI proteins (NFI-C), reduced the occupancy of predicted sites, however at the same time indicating that cells could compensate the missing protein with the other members of the family. Keywords: ChIP-Seq (chromatin immunoprecipitation and high throughput sequencing) ChIP-Seq (chromatin immunoprecipitation and high throughput sequencing) using antibody against NFI family of transcription factors in two cell types (wild type and NFI-C knock-out mouse embryonic fibroblasts MEFs)

2010-04-24 | E-GEOD-15844 | biostudies-arrayexpress

Cerebellar Granule Neuron Temporal-NFI Microarray Data

Project description:Dendrite and synapse development are critical for establishing appropriate neuronal circuits, and disrupted timing of these events can alter connectivity leading to disordered neural function. In early postnatal development of cerebellar granule neurons (CGNs), the expression of many genes is temporally regulated. Further, NFI (Nuclear Factor I) proteins have been shown to play important roles in the regulation of gene expression in developing CGNs. To identify NFI-regulated genome-wide targets involved in late maturation of mouse CGNs, we performed two groups of microarray expression analysis: (1) temporal expression arrays using 1.5 and 6 day cultures of mouse CGNs representing immature and more mature CGNs, respectively, which identified 844 Temporal-Up or Down genes; and (2) NFI-regulated genes in 6 day CGN cultures that were infected at the time of plating with lentiviral vectors expressing either NFI dominant repressor (NFI-EnR) or EnR control protein. This identified 686 NFI-Up (NFI-EnR down-regulated) or NFI-Down (NFI-EnR up-regulated) genes. Overlap analysis identified 212 temporal genes that were regulated by NFI. These results indicated that NFI plays a pivotal role in the regulation of late CGN maturation.

2012-11-07 | GSE42018 | GEO

Cerebellar Granule Neuron Temporal-NFI Microarray Data

2012-11-07 | E-GEOD-42018 | biostudies-arrayexpress

Genome-wide mapping of Nuclear Factor I binding sites using ChIP-Seq in WT and NFI-C knock-out MEFs

2010-04-24 | GSE15844 | GEO

ChIP-chip analysis of NFI-1 in wildtype (N2) mixed stage C. elegans

Project description:The conserved Nuclear Factor I (NFI) family of transcription factors is unique to animals and essential for mammalian development. The C. elegans genome encodes a single NFI family member, whereas vertebrate genomes encode four distinct NFI protein subtypes (A, B, C, and X). NFI-1 deficient worms exhibit abnormalities including reduced lifespan, defects in movement and pharyngeal pumping, and delayed egg-laying. To explore the functional basis of these phenotypes, we sought to comprehensively identify NFI-1 binding targets in C. elegans. We first established NFI-1 DNA-binding specificity using an in vitro DNA-selection strategy. Analysis yielded a consensus motif of TTGGCA(N3)TGCCAA, which occurs 586 times in the genome, a 100-fold higher frequency than expected. We next asked which sites were occupied by NFI-1 in vivo by performing chromatin immunoprecipitation of NFI-1 followed by microarray hybridization (ChIP-chip). Only 55 genomic locations were identified, an unexpectedly small target set. In vivo NFI-1 binding sites tend to be upstream of genes involved in core cellular processes such as chromatin remodeling, mRNA splicing, and translation. Remarkably, 67/80 (84%) of the C. briggsae homologs of the identified targets contain conserved NFI binding sites in their promoters. These experiments provide a foundation for understanding how NFI-1 is recruited to unexpectedly few in vivo sites to perform its developmental functions, despite a vast over-representation of its binding site. To our knowledge, this represents the first genome-wide location study of any transcription factor in C. elegans, and the first genome-wide analysis in any species of an NFI transcription factor. 4 biological replicates of NFI-1 ChIP-chip (including 1 dye-swap) were performed with 2 pre-immune Mock ChIP-chip controls from corresponding extracts.

2009-01-30 | E-GEOD-13918 | biostudies-arrayexpress

Response to TGFB in colon fibroblasts

Project description:We obtained gene expression signatures from TGF-beta treated fribroblasts. Upregulated genes predict poor prognosis in Colorectal Cancer. Fibroblasts extracted from human normal colon mucosa were treated with TGF-Î²1 for 8 hours. Gene expression profiles for treated or untreated fibroblasts were measured in duplicate using HG-133+PM Affimetrix arrays.

2015-01-28 | E-GEOD-64192 | biostudies-arrayexpress

Whole-genome microarray analysis of human skin fibroblasts

Project description:Connective tissue growthfactor (CTGF/CCN2) is a matricellular protein induced by transforming growth factor-beta (TGF-beta) and intimately involved with tissue repair and overexpressed in various fibrotic conditions. We have previously shown that keratinocytes in vitro downregulate TGF-beta induced expression of CTGF in fibroblasts by an interleukin-1 alfa (IL-1alfa) dependent mechanism. With this study we want to get a better overall perspective who fibroblasts respond on TGF-beta and in a TGF-Beta stinulated system, what effect addition of IL-1 alfa have. This to understand the expression of CTGF in human fibroblasts which in turn have implications for the pathogenesis of fibrotic conditions involving the skin. Microarray was performed on human skin fibroblast RNA from one patient, Fibroblasts were seeded in vitro as a control (Control, C), TGF-beta were added to fibroblasts and incubated for 16 h (addition of TGF-beta, T) and both IL-1alfa and TGF-beta were added to fibroblasts for 16 h (addition of IL-1alfa and TGF-beta, IT). Each condition (C,T and IT) were done in three replicates.

2016-04-14 | E-GEOD-69447 | biostudies-arrayexpress

Microarray data for rejuvenation experiments through reprogramming

Project description:Proliferative and replicative senescent fibroblasts from aged human donors were reprogrammed towards pluripotency and re-differentiated in fibroblasts and then further analyzed for rejuvenation assessment. Comparison of microarrays were performed by non hierarchical clustering visualized in with Treeview software

2011-12-14 | E-GEOD-27924 | biostudies-arrayexpress

Microenvironment-driven resistance to B-Raf inhibition in a melanoma patient is accompanied by broad changes of gene methylation and expression in distal fibroblasts. Genome methylation study.

Project description:In this study, we compared gene expression and genome methylation of diverse fibroblast populations from a patient suffering from acrolentiginous melanoma (Breslow 4.0 mm, Clark IV, B-Raf V600E mutated). Stromal cells from the metastasis, i.e., melanoma associated fibroblasts (MAF), were positive for smooth muscle actin (SMA). Autologous control fibroblasts (ACF) isolated from distant uninvolved skin of the same patient during B-Raf inhibitor therapy and before clinical progression of the disease exhibited also strong SMA expression. Similar phenotype was observed in control dermal fibroblasts (CDF) from different donors yet exclusively after stimulation by TGF-Î²1. The identified differences in gene transcription as well as in DNA methylation indicate systemic activation of dermal fibroblasts in a patient with malignant melanoma. This dataset contains genome methylation profiling data, complementary transcriptome profiling data are available under accession E-MTAB-4964.

2018-12-30 | E-MTAB-4965 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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