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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The role of Foxp1/4 in lung development

ABSTRACT: Foxp1/4 transcription factors are conserved transcriptional repressors expressed in overlapping patterns during lung development as well as in the adult lung. However, the role of Foxp1/4 in development and homeostasis of the pseudostratified epithelium of the proximal airways and trachea is unknown. We propose to determine the roles for Foxp1/4 in lung development by deleting these genes in lung epithelial specific knockout mice. To explore the genome wide consequences of Foxp1/4 deficiency on secretory epithelial differentiation in the lung, we performed microarray analysis of Shh- cre control and Foxp1/4ShhcreDKO mutants lungs at E14.5, 3 embryos, respectively.

ORGANISM(S): Mus musculus

SUBMITTER: Shanru Li

PROVIDER: E-GEOD-34584 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Foxp1/4 control epithelial cell fate during lung development and regeneration through regulation of anterior gradient 2.

Li Shanru S Wang Yi Y Zhang Yuzhen Y Lu Min Min MM DeMayo Francesco J FJ Dekker Joseph D JD Tucker Philip W PW Morrisey Edward E EE

Development (Cambridge, England) 20120606 14

The molecular pathways regulating cell lineage determination and regeneration in epithelial tissues are poorly understood. The secretory epithelium of the lung is required for production of mucus to help protect the lung against environmental insults, including pathogens and pollution, that can lead to debilitating diseases such as asthma and chronic obstructive pulmonary disease. We show that the transcription factors Foxp1 and Foxp4 act cooperatively to regulate lung secretory epithelial cell ...[more]

PMID: 22675208

Similar Datasets

The role of Foxp1/4 in lung development

Project description:Foxp1/4 transcription factors are conserved transcriptional repressors expressed in overlapping patterns during lung development as well as in the adult lung. However, the role of Foxp1/4 in development and homeostasis of the pseudostratified epithelium of the proximal airways and trachea is unknown. We propose to determine the roles for Foxp1/4 in lung development by deleting these genes in lung epithelial specific knockout mice.

2012-08-02 | GSE34584 | GEO

Knockdown of FOXP1 promotes the development of lung adenocarcinoma

Project description:Lung cancer is one of the most common cancers in the world, which accounts for about 27% of all cancer deaths. However, the mechanisms underlying the pathogenesis of lung cancer cells remain largely elusive. In this study, we examined the role of the Forkhead box protein P1 (FOXP1) in lung cancer development. Our Oncomine analysis shows that FOXP1 is downregulated in lung adenocarcinoma compared with normal lung tissue. Knockdown of FOXP1 promotes the proliferation growth and invasion of PC9 and A549 cells by regulating genes of chemokine signaling molecules, including CCR1, ADCY5, GNG7, VAV3, and PLCB1. Simultaneous knockdown of CCR1 and FOXP1 attenuated FOXP1 knockdown-induced increase of lung cancer cell growth. Finally, knockdown of FOXP1 in PC9 cells promotes the tumorigenesis via CCR1 signaling in xenograft mouse model. Taken together, our data suggest that FOXP1 plays important roles in preventing lung adenocarcinoma development via suppressing chemokine signaling pathways. Novel strategies might be developed to prevent the development of lung adenocarcinoma by targeting FOXP1

2018-02-10 | GSE108500 | GEO

The role of Foxp1/2/4 in lung endoderm identity

Project description:Our previous work has demonstrated an important role for the Foxp1/2/4 subfamily of transcriptional repressors in promoting lung epithelial differentiation. However, the overall role of this transcription factor subfamily in early lung endoderm identity is unknown.

2017-01-02 | GSE64777 | GEO

Knockdown of FOXP1 promotes the development of lung adenocarcinoma

Project description:Knockdown of FOXP1 promotes the development of lung adenocarcinoma

| PRJNA427471 | ENA

Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

Project description:Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls. We generated Ezh2 epithelial mutant lungs by crossing the Ezh2-floxed line (Su et al., 2003) with the Shh-cre line (Harfe et al., 2004). We isolated RNA from whole mouse lungs at embryonic day 14.5 from 4 Shh-cre:Ezh2-flox/flox embryos (M1-M4) and 4 Shh-cre embryos (C1-C4). Littermates are as follows: C1+C2; C3+C4; M1+M2; M3+M4.

2015-02-04 | E-GEOD-60660 | biostudies-arrayexpress

Role of Fzd2 in lung epithelium development

Project description:Fzd2 is a Wnt receptor expressed in the embryonic lung. We made a conditional knockout of Fzd2 to specifically address the role of signaling through Fzd2 in lung epithelial development. To explore the genes that are regulated by signaling through the Fzd2 receptor in the lung epithelium, we performed microarray analysis of Shhcre control and Fzd2CKO lungs at E12.5

2014-07-29 | E-GEOD-49370 | biostudies-arrayexpress

Non-IG Aberrations of FOXP1 in B-Cell Malignancies Lead to an Aberrant Expression of N-Truncated Isoforms of FOXP1

Project description:The transcription factor FOXP1 is implicated in the pathogenesis of B-cell lymphomas through immunoglobulin heavy chain (IGH) locus-related chromosomal translocations leading to dysregulated expression of FOXP1. Translocations of FOXP1 with non-IG gene sequences have been also reported, but the molecular consequences of such aberrations remain undetermined. Here, using molecular cytogenetics and molecular biology studies, we comprehensively analyzed four lymphoma cases with non-IG rearrangements of FOXP1 and compared these with cases harboring t(3;14)(p13;q32)/IGH-FOXP1 and FOXP1-expressing lymphomas without underlying t(3p13/FOXP1). We found that non-IG rearrangements are usually acquired during evolution of lymphoma and constantly target the coding region of FOXP1, promiscuously fusing with coding and non-coding gene sequences at various reciprocal breakpoints (2q36, 10q24 and 3q11). Intriguingly, these rearrangements do not generate functional chimeric genes but commonly disrupt the full-length FOXP1 transcript leading to an aberrant expression of N-truncated FOXP1 isoforms, as shown by QRT-PCR and Western blot analysis. In contrast, cases with t(3;14)(p13;q32)/IGH-FOXP1 overexpress the full-length FOXP1. Collectively, our findings point to a dual mechanism through which FOXP1 is implicated in B-cell lymphomagenesis. The primary t(3;14)(p13;q32)/IGH-FOXP1 produces the full-length protein with potent oncogenic activity, whereas the secondary non-IG 17 rearrangements of FOXP1 generate N-truncated FOXP1 isoforms, likely driving progression of disease. Using molecular cytogenetics and molecular biology studies (including RNA-seq), we comprehensively analyzed four lymphoma cases with non-IG rearrangements of FOXP1 and compared these with cases harboring t(3;14)(p13;q32)/IGH-FOXP1 and FOXP1-expressing lymphomas without underlying t(3p13/FOXP1).

2013-09-04 | E-GEOD-50514 | biostudies-arrayexpress

Human nasopharyngeal cancer cell HONE1 FOXP1 immunoprecipitates LC-MS

Project description:Identification of peptides matching to LCK in FOXP1 immunoprecipitates from HONE1 cells by mass spectrometry

2022-04-04 | PXD031014 | Pride

Gene expression changes in stimulated and unstimulated Foxp1-deficient B cells.

Project description:Foxp1 is expressed throughout B cell development, but the physiological functions in mature B lymphocytes are unknown. We therefore evaluated differential gene expression in Foxp1-deficient B cells, with or withouth IgM stimulation.

2018-02-19 | GSE85240 | GEO

FOXP1 orchestration of ASD-relevant signaling pathways.

Project description:Mutations in the gene encoding the transcription factor forkhead box P1 or FOXP1 occur in patients with neurodevelopmental disorders, including autism. However, the function of FOXP1 in the brain remains mostly unknown. Here, we identify the gene expression program regulated by FoxP1 in both human neural cells and mouse brain and demonstrate a conserved role for FOXP1 transcriptional regulation of autism and Fragile X Mental Retardation Protein (FMRP) mediated pathways. Coexpression networks support a role for Foxp1 in neuronal activity, and we show that Foxp1 is necessary for neuronal excitability. Using a Foxp1 mouse model, we observe defects in ultrasonic vocalizations. This behavioral phenotype is reflected at the genomic level as striatal Foxp1-regulated overlap with genes known to be important in rodent vocalizations. These data support an integral role for FOXP1 in regulating signaling pathways vulnerable in developmental disorders and the specific regulation of pathways important for vocal communication. We carried out RNA-sequencing (RNA-seq) and ChIP-sequencing of human neural progenitors cells. We carried out RNA-sequencing (RNA-seq) of mouse striatal tissue, mouse hippocampal tissue and mouse cortical tissue. For the RNA-seq, four indipendent replicates were used for the neural progenitor cells and mouse tissues. For the Chip-seq, a single neural progenitor cell line was used.

2015-10-26 | E-GEOD-62718 | biostudies-arrayexpress

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