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RNA-Seq analysis of NKX2.2 knockdown in human pancreatic islets

ABSTRACT: Aim: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

ORGANISM(S): Homo sapiens

PROVIDER: GSE79724 | GEO | 2016/12/20

SECONDARY ACCESSION(S): PRJNA316850

REPOSITORIES: GEO

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RNA-Seq analysis of the pancreatic islets of beta cell specific adult Nkx2.2 mutant mice

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2016-12-20 | GSE79723 | GEO

RNA-Seq analysis of E15.5 pancreas of both whole body Nkx2.2 mutant embryos and endocrine progenitor specific Nkx2.2 mutant embryos

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2017-01-09 | GSE80444 | GEO

RNAseq analysis of the colon of intestine-specific adult Nkx2.2 mutant mice

Project description:Aim: Transcriptional analysis of the colon of adult Nkx2.2flox/flox;Villin-Cre (Nkx2.2int) mice versus control Methods: 2 cm of the colon (as measured after the caecum) of 6 week old control and mutant mice 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. Results: 53 genes with a p-value <0.05 were down-regulated and 36 were up-regulated. Among the changed genes are enteroendocrine hormones. Conclusion: Nkx2.2 regulates enteroendocrine cell specification

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RNAseq analysis of the duodenum of intestine-specific adult Nkx2.2 mutant mice

Project description:Aim: Transcriptional analysis of the duodenum of adult Nkx2.2flox/flox;Villin-Cre (Nkx2.2int) mice versus control Methods: 2 cm of the duodenum (as measured from the stomach) of 6 week old control and mutant mice 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. Results: 184 genes with a p-value <0.05 were down-regulated and 211 were up-regulated. Among the down-regulated genes are most enteroendocrine hormones. Conclusion: Nkx2.2 regulates enteroendocrine cell specification

2016-07-28 | GSE72761 | GEO

RNAseq analysis of the duodenum of intestine-specific adult Nkx2.2 mutant mice

2016-07-28 | E-GEOD-72761 | biostudies-arrayexpress

RNAseq analysis of the colon of intestine-specific adult Nkx2.2 mutant mice

2016-07-28 | E-GEOD-78902 | biostudies-arrayexpress

NKX2.2

Project description:NKX2.2

| PRJNA316849 | ENA

RNA Seq analysis of e12.5 mouse pancreatic buds from control and Pdxcre; Gata4fl/fl;Gata6fl/fl; Tom mice

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2016-03-08 | E-GEOD-77083 | biostudies-arrayexpress

Global profiling of Nkx2.2 SD-domain mutant pancreas during development and adulthood compared to transcriptional profiling of SD-domain mutant expressing neural progenitors.

Project description:The consolidation of unambiguous cell fate commitment relies on the ability of transcription factors (TFs) to exert tissue-specific regulation of complex genetic networks. The mechanisms by which TFs establish such precise control over gene expression, however, have remained elusive—especially in instances where a single TF operates in two or more discrete cellular systems. In this study, we demonstrate that  cell specific functions of NKX2.2 are driven by the highly conserved NK2-Specific Domain (SD). Mutation of the endogenous NKX2.2 SD domain prevents the developmental progression of beta cell precursors into mature, insulin-expressing beta cells, resulting in overt neonatal diabetes. Within the adult beta cell, the SD domain stimulates beta cell performance through the activation and repression of a subset of NKX2.2-regulated transcripts critical for beta cell function. These irregularities in beta cell gene expression may be mediated via SD domain-contingent interactions with components of the nuclear pore complex. In stark contrast to these pancreatic phenotypes, however, the SD domain is entirely dispensable for the development of NKX2.2-dependent cell types within the CNS. Together, these results reveal a previously undetermined mechanism through which NKX2.2 directs disparate transcriptional programs in the pancreas vs. neuroepithelium.

2024-02-21 | GSE226345 | GEO

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2009-11-05 | E-CBIL-44 | biostudies-arrayexpress

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