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Mesenchymal Nuclear factor I B regulates cell proliferation and epithelial differentiation during lung maturation

ABSTRACT: We generated Nfibf/f mice and then cross with Dermo1-Cre mice to obtain Nfibf/f, Dermo1-Cre mice. In these Nfibf/f, Dermo1-Cre mice, there are defects in sacculation and epithelial cell differentiation. We performed micoarray analysis to find the genes which are possibley regulated by NFI-B and related to lung maturation during lung development.

ORGANISM(S): Mus musculus

PROVIDER: GSE24465 | GEO | 2011/09/29

SECONDARY ACCESSION(S): PRJNA132759

REPOSITORIES: GEO

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Mesenchymal Nuclear factor I B regulates cell proliferation and epithelial differentiation during lung maturation

Project description:We generated Nfibf/f mice and then cross with Dermo1-Cre mice to obtain Nfibf/f, Dermo1-Cre mice. In these Nfibf/f, Dermo1-Cre mice, there are defects in sacculation and epithelial cell differentiation. We performed micoarray analysis to find the genes which are possibley regulated by NFI-B and related to lung maturation during lung development. We used microarrays to performing transcriptional profiling of Nfibf/f, Dermo1-Cre and Nfibf/f lungs at E18.5

2011-09-28 | E-GEOD-24465 | biostudies-arrayexpress

Mesenchymal nuclear factor I B regulates cell proliferation and epithelial differentiation during lung maturation.

Project description: Not available

| S-EPMC3098902 | biostudies-literature

Gene expression profile of E18.5 mouse lungs lacking epithelial Hdac3

Project description:The molecular mechanism of how lung sacculation occurs is poorly understood. Loss of epithelial Hdac3 results in defects in the proper expansion of distal lung saccules into primitive alveoli. In this microarray, we seek to investigate the gene profile changes caused by loss of Hdac3 to better understand the molecular pathways that are regulated by Hdac3 during lung sacculation.

2016-06-21 | GSE70684 | 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

The NFIB/CARM1 Partnership is a Therapeutic Target for Small Cell Lung Cancer

Project description:This project identified NFI family members as CARM1 substrates. NFIB was previously reported to play a critical role in the development of small cell lung cancer. We provided evidence that the arginine methylation of NFIB is required for its oncogenic function in small cell lung cancer.

2023-02-07 | PXD038237 | Pride

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

Investigation of the gene expression changes triggered by the lung mesenchymal Tsc2KO in each major cell subpopulation of the adult mouse lung

Project description:Tumor suppressor Tuberous sclerosis complex 2 (TSC2) is a key negative regulator of mammalian target of rapamycin (mTOR), a central controller of cell growth and metabolism in health and disease. Loss of TSC2 induces the constitutive activation of mTORC1 in rare lung disease pulmonary Lymphangioleiomyomatosis (LAM), which affects only women of childbearing age and characterized by lung destruction and progressive loss of pulmonary function. Little is known how TSC2 loss induces LAM and what is the LAM cell of origin. To determine cell-type specific effects of TSC2 loss and mTORC1 activation on lung homeostasis we generated new transgenic mice with targeted Tsc2 deletion in lung mesenchyme Tbx4-Cre+Tsc2flox/flox and lung epithelium Shh-Cre+Tsc2flox/flox. Both Tbx4-Cre+, Tsc2flox/flox and Shh-Cre+, Tsc2flox/flox mice were viable and fertile. Adult Tbx4-Cre+Tsc2flox/flox mice demonstrated mTORC1 activation in lung mesenchyme, progressive alveolar enlargement, female-specific pulmonary function decline and prgenancy-induced lesion growth. To investigate molecular mechanism underlying observed phenotypic changes in the Tsc2KO lungs we performed comparative bulk-RNAseq analysis of the gene expression changes in the major cell subpopulations of the adult female 8-week-old Tsc2KO mouse lungs compared to the age- and sex-matched WT controls.

2020-08-31 | GSE139818 | GEO

Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (miRNA expression)

Project description:We constructed LSL-KrasG12D/+ and Spc-Cre;LSL-KrasG12D/+ mice to investigate the role of microRNA in the pathogenesis of lung cancer

2019-06-30 | GSE132096 | GEO

The orphan nuclear receptor TR4 regulates erythroid cell proliferation and maturation.

Project description: Not available

| S-EPMC5721283 | biostudies-literature

Smad1 and its target gene Wif1 coordinate BMP and Wnt signaling activities to regulate lung development

Project description:Bone morphogenetic protein 4 (BMP4) is essential for lung development. To define its intracellular signaling mechanisms by which BMP4 regulates lung development, BMP-specific Smad1 or Smad5 was selectively knocked out in fetal mouse lung epithelial cells. Abrogation of lung epithelial-specific Smad1, but not Smad5, resulted in retardation of lung branching morphogenesis and reduced sacculation, accompanied by altered distal lung epithelial cell proliferation and differentiation, and consequently severe neonatal respiratory failure. By combining cDNA microarray with ChIP-chip analyses, Wnt inhibitory factor-1 (Wif1) was identified as a novel target gene of Smad1 in the developing mouse lung epithelial cells. Loss of Smad1 transcriptional activation of Wif1 expression was associated with reduced Wif1 expression and increased Wnt/beta-catenin signaling activity in lung epithelia, resulting in specific fetal lung abnormalities. Therefore, a novel regulatory loop of BMP4-Smad1-Wif1-Wnt/beta-catenin in coordinating BMP and Wnt pathways to control fetal lung development is suggested. mRNA profiling: Total RNA was isolated from left lobe lungs of three pair of E18.5 wild type and Smad1 lung epithelium-specific conditional knockout mice

2011-01-07 | E-GEOD-26502 | biostudies-arrayexpress

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