RNA-seq profiling of transcriptomes of control and Hif1a mutant E12.5 hearts
Ontology highlight
ABSTRACT: Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts 6 total RNAseq runs with 3 experimental samples and 3 controls samples
Project description:Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts
Project description:Purpose: to identify genes directly bound by HIF1a in cardiomycoytes Methods: crosslinked chromatin isolated from E12.5 mouse hearts was precipitated using an anti-HIF1a antibody and processed for sequencing. A list of genes containing a HIF1a peak (Minimum score 3.5) was compared with RNA-seq results to identify genes that are bound by HIF1a and expressed in E12.5 hearts Results: this analysis identified 1016 genes expressed and bound by HIF1a in embryonic hearts
Project description:To understand the underlying mechanism by which the Hif1a gene is required by hematopoietic stem cells (HSCs), we performed a comparative DNA microarray analysis using total RNA isolated from wild type Lin-Sca-1+c-Kit+ cells and Hif1a-/- Lin-Sca-1+c-Kit+ cells. The result was validated by quantitative real-time PCR analysis of wild type Lin-Sca-1+c-Kit+ and Hif1a-/- Lin-Sca-1+c-Kit+ cells. We compared the gene profile of HSCs between WT mice and Hif1a-/- mice.
Project description:In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed RNA-seq. 11389 and 7767 genes were regulated by KIMAT1 and HIF1A-As2, respectively.
Project description:In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed small RNA-seq. 214 and 233 microRNAs were regulated by KIMAT1 and HIF1A-As2, respectively.
Project description:We and others have previously shown FOXA1 is frequently mutated or downregulated in castration resistant prostate cancer (CRPC). Here we report a novel role for transcription factor FOXA1 in directly repressing HIF1A expression in prostate cancer cells. FOXA1 knockdown induced the expression of HIF1A and hypoxia signature genes, which were reduced by concomitant HIF1A knockdown or treatment with HIF1A inhibitor KC7F2. Thus, our data suggest FOXA1 loss induces aberrant hypoxia signaling and tumor progression in part via HIF1A.
Project description:To understand the underlying mechanism by which the Hif1a gene is required by hematopoietic stem cells (HSCs), we performed a comparative DNA microarray analysis using total RNA isolated from wild type Lin-Sca-1+c-Kit+ cells and Hif1a-/- Lin-Sca-1+c-Kit+ cells. The result was validated by quantitative real-time PCR analysis of wild type Lin-Sca-1+c-Kit+ and Hif1a-/- Lin-Sca-1+c-Kit+ cells.
Project description:We report the application of chromatin immunoprecipitation and next generation sequencing technology for HIF1a binding sites at genome wide level in a RCC (renal cell carcinoma) cell line under hypoxia conditions. We found HIF1a binding sites in Caki-2 cell line under hypoxia conditions. Especially, we found HIF1a bind to SPOP under hypoxia condition, which was further validated. Examination of HIF1a binding sites in Caki-2 cell line under hypoxia condition