Mouse ESCs depleted of the epigenetic modifying enzyme Usp22 fail to differentiate properly. Ectopic expresison of Usp22 results in spontaneous differnetiation.
The epigenetic modifier ubiquitin-specific protease 22 (USP22) regulates embryonic stem cell differentiation via transcriptional repression of sex-determining region Y-box 2 (SOX2).
Cell line, Treatment
View SamplesSingle-cell RNA-seq (Smart-Seq2) to profile of cardiac progenitor cells Overall design: Transcriptional profiling of cultured CPCs was performed by scRNA-Seq approaches using Smart-Seq2 technology
In situ transcriptome characteristics are lost following culture adaptation of adult cardiac stem cells.
Specimen part, Subject
View SamplesBulk RNA-seq to profile of c-kit+ cardiac interstitial cells, comparing the transcriptomes of Pim-1 enhanced cardiac progenitor cells and transfection control Overall design: Transcriptional profiling of Pim-1 enhanced human derived cardiac interstitial cells by bulk RNA-Seq
Safety profiling of genetically engineered Pim-1 kinase overexpression for oncogenicity risk in human c-kit+ cardiac interstitial cells.
Specimen part, Subject
View SamplesWe recently found that the endoplasmic reticulum (ER) stress response (ERSR) is activated in surviving cardiac myocytes in a mouse model of in vivo myocardial infarction. ATF6 is an ER stress-activated transcription factor that induces ERSR genes, some of which encode proteins that may protect against ischemic damage. However, few ERSR genes have been identified in the heart, and there have been no gene expression profiling studies of ATF6-inducible genes, in vivo. We previously generated transgenic (TG) mice that express tamoxifen-activated ATF6, ATF6-MER, in the heart; ATF6-MER conferred tamoxifen-dependent ATF6 activation and protection from ischemic damage. To understand of the mechanism of ATF6-mediated cardioprotection, gene expression profiling of ATF6-MER TG mouse hearts was performed. Activated ATF6 changed expression levels of 1,162 genes in the heart; of the 775 ATF6-inducible genes, only 23 are known ERSR genes. One of the genes not expected to be induced by ATF6 is modulatory calcinuerin-interacting protein-1 (MCIP1). MCIP1 is induced in a calcineurin/NFAT-dependent manner during myocardial hypertrophy and it can feedback inhibit cardiomyocyte growth. We found that MCIP1 expression in cultured cardiomyocytes was increased by the prototypical ER stresser, tunicamycin (TM), or by simulated ischemia. Moreover, infecting cardiomyocytes with adenovirus encoding activated ATF6 induced MCIP1 expression and inhibited myocyte growth in response to the alpha 1-adrenergic agonist, phenylephrine. These results suggest that MCIP1 can be induced in the heart by ER stresses, such as ischemia. Moreover, b integrating hypertrophy and ER stress, MCIP-modulated myocyte growth may help rejuvenate nascent ER protein folding, which could contribute to protection from ischemic damage.
Coordination of growth and endoplasmic reticulum stress signaling by regulator of calcineurin 1 (RCAN1), a novel ATF6-inducible gene.
Sex, Age, Specimen part, Treatment
View SamplesObjectives: We studied the signal transduction of atrial structural remodelling that contributes to
Rac1-induced connective tissue growth factor regulates connexin 43 and N-cadherin expression in atrial fibrillation.
Specimen part
View Samplesabout 250 genes were significantly changed after Gata4 and Gata6 were specifically deleted in the pancreatic progenitor cells Overall design: 6 pancreatic buds were pooled for the control, and 12 pancreatic buds were pooled for the Pdxcre; Gata4fl/fl; Gata6fl/fl. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq
GATA4 and GATA6 regulate pancreatic endoderm identity through inhibition of hedgehog signaling.
Specimen part, Disease, Subject
View SamplesSingle-cell RNA-seq (10X Genomics Chromium) to profile of cardiac progenitor cells, comparing the transcriptomes of diploid and tetraploid cardiac progenitor cells Overall design: Transcriptional profiling of diploid and tetraploid CPCs by scRNA-Seq approaches using 10X Genomics Chromium
Cardiac interstitial tetraploid cells can escape replicative senescence in rodents but not large mammals.
Sex, Specimen part, Cell line, Subject
View SamplesWe report the transcriptome changes that result of the genomic deletion of one or two alleles of an islet-specific long non-coding RNA (Blinc1) in isolated pancreas from e15.5 mouse embryos. Overall design: Pancreas from e15.5 embryos were dissected and total RNA extracted. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq.
βlinc1 encodes a long noncoding RNA that regulates islet β-cell formation and function.
Specimen part, Subject
View SamplesAim:Transcriptional analysis of NKX2.2 knockdown versus control in human pancreatic islets Methods:Pancreatic islets from 3 human donors were transduced with an adenovirus encoding an shRNA directed against human NKX2.2 or a scrambled shRNA control. Total RNA was extracted.Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the human genome (Human: NCBI/build37.2)) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: Among the dysregulated genes with a p-value=0.05 are important genes for the maintenance of beta cell function and idenity. Conclusion: Nkx2.2 is a critical regulator of beta cell function and identity Overall design: mRNA profiles of the pancreatic islets from 3 human donors transduced with Ad.sh-NKX2.2 or scramble sh-RNA control vector were generated by deep sequencing , using Illumina HiSeq2000.
Genetic evidence that Nkx2.2 acts primarily downstream of Neurog3 in pancreatic endocrine lineage development.
Specimen part, Subject
View SamplesAim:Transcriptional analysis of the pancreatic islets of adult Nkx2.2 flox/flox; RipCre mice versus control Methods:Pancreatic islets from 4week old Nkx2.2 mutant mice and controls were isolated and total RNA was extracted.Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq. Results: Among the downregulated genes with a p-value=0.05 are important genes for beta cell function and idenity.Among the upregulated genes with a p-value=0.05 are non beta endocrine hormones. Conclusion: Nkx2.2 activates important beta cell genes and actively represses non beta cell genes Overall design: mRNA profiles of the pancreatic islets of 4 week old control and Nkx2.2 mutant mice were generated by deep sequencing , in triplicate, using Illumina HiSeq2000.
Genetic evidence that Nkx2.2 acts primarily downstream of Neurog3 in pancreatic endocrine lineage development.
Specimen part, Subject
View Samples