Similar Datasets
Project description:We report the identification of genome-wide binding site of the cardiac transcription factor Nkx2-5 during mouse heart development. Examination of Nkx2-5 binding in wild-type mouse in duplicate.
2015-09-02 | E-GEOD-44574 | biostudies-arrayexpress
Project description:We report the identification of genome-wide binding site of the cardiac transcription factor Nkx2-5 during mouse heart development.
2015-09-02 | GSE44574 | GEO
Project description:ChIP-seq was performed to identify the binding regions of SPDEF and NKX2-1 in A549 lung carcinoma cells expressing NKX2-1 and SPDEF.
2017-03-02 | GSE86957 | GEO
Project description:RNA-seq was performed to identify genes affected by CRISPRi (dCas9-KRAB) with sgRNA (sgSFTPB#2) targeting the first intronic region of human SFTPB bound by NKX2-1 in an unbiased genome-wide fashion using A549 lung carcinoma cells that constitutively express dCas9-KRAB and NKX2-1.
2021-03-25 | GSE162186 | GEO
Project description:We conducted a genome-wide analysis to identify regulatory variants affecting the binding of NKX2-5, a core cardiac development transcription factor, and investigated their role in cardiac gene expression and EKG phenotypes. We generated iPSC-derived cardiomyocytes (iPSC-CMs) from a pedigree of seven whole-genome sequenced individuals, and profiled them with a variety of functional genomic assays including RNA-Seq, ATAC-Seq, and ChIP-Seq of both histone modification H3K27ac and NKX2-5. After establishing that iPSC-CMs recapitulated cardiomyocyte-specific expression and epigenetic signatures, and that genetic variants affected the variability of molecular phenotypes across the iPSC-CM lines, we identified heterozygous sites that showed allele-specific effects (ASE). We then investigated NKX2-5 ASE variants in detail by examining whether they altered cardiac TF motifs, and whether they were enriched for eQTLs and EKG GWAS-SNPs. Our data reveal that variation affecting the binding of NKX2-5 and other cardiac TFs likely serves as a molecular mechanism underlying control of numerous EKG loci across the genome, and that fine-mapping approaches, combined with molecular phenotype data from iPSC-CMs, can be used to prioritize causal variants in EKG GWAS loci.
2019-07-12 | GSE133833 | GEO
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas. NKX2-1 ChIP-seq from three lung adenocarcinoma cell lines with amplification of NKX2-1
2013-01-22 | E-GEOD-39998 | biostudies-arrayexpress
Project description:Although Thyroid transcription factor-1 (TTF-1, encoded by NKX2-1 gene) is highly expressed in small cell lung carcinoma (SCLC) and lung adenocarcinoma (LADC), difference in the functional roles of TTF-1 between SCLC and LADC remains to be elucidated. The aim of this study was to clarify the differences in the TTF-1 binding regions and functional roles in SCLC and LADC. Employing chromatin immunoprecipitation-sequencing (ChIP-seq) , here we compared the genome-wide TTF-1-binding profiles and the TTF-1-mediated transcriptional programs in a SCLC and a LADC cell lines. We also investigated ASCL1 binding regions in SCLC cells.
2019-11-30 | GSE139868 | GEO
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas.
2013-01-22 | GSE39998 | GEO
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas.
2013-04-15 | GSE40270 | GEO
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas. NCI-H2009 cells with stable expression of either pLKO-Tet-Op-shGFP (n=4) or pLKO-Tet-Op-shNKX2-1 (pooled population; n=3 and a clone; n=3) were treated with 50ng/ml of doxycyline for 48 hours. Total RNA was extracted, gene expression profiling was performed and differential gene expression between shGFP and shNKX2-1 was analyzed to determine the effects by suppression of NKX2-1 in NCI-H2009 cells.
2013-04-15 | E-GEOD-40270 | biostudies-arrayexpress