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NKX2.2

ABSTRACT: NKX2.2

PROVIDER: PRJNA316849 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3313320.fastq.gz	Fastqsanger.gz
	SRR3313330.fastq.gz	Fastqsanger.gz
	SRR3317150.fastq.gz	Fastqsanger.gz
	SRR3313321.fastq.gz	Fastqsanger.gz
	SRR3313331.fastq.gz	Fastqsanger.gz

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

Project description:Aim: Transcriptional analysis of E15.5 whole pancreas of Nkx2.2-LacZ/LacZ embryos versus control and Ngn3-Cre; Nkx2.2-flox/flox embryos versus control Methods: Embryonic pancreata were isolated at E15.5 from Nkx2.2 mutant mice and controls. 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: There is significant overlap between the differentially expressed genes of whole body Nkx2.2 mutant embryos and endocrine progenitor specific Nkx2.2 mutant embryos; many of the downregulated genes (p-value < 0.05) are genes involved in beta cell function. Conclusion: Nkx2.2 functions within the endocrine progenitor lineage to activate beta cell genes

2017-01-09 | GSE80444 | GEO

Identification of dysregulated transcripts in nkx2.2(RNAi) planarians.

Project description:Nkx2.2 is an intestine-enriched transcription factor required for regeneration in planarians. The goal of this study was to identify differentially expressed transcripts in uninjured nkx2.2(RNAi) planarians.

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Genome-wide disclosure of the Nkx2.2 targets in oligodendrocytes and their progenitor cells suggests several novel target genes

Project description:The Nkx2.2 transcription factor contributes to regulate the timing of myelination in the CNS. Still, information about the regulon of Nkx2.2 in oligodendrocytes (Ols) and their progenitor cells (OPCs) is restricted to a few genes. Therefore we aimed to identify the entire regulon of Nkx2.2. We performed transcript profiling of postnatal Nkx2.2-/- mice, investigated the expression of selected transcripts in Ol lineage cells after siRNA induced Nkx2.2 knock-down, and identified the genome-wide active Nkx2.2 binding sites in murine OPCs and Ols by use of ChIP-sequencing technique. Thereby we have found 521 genes with active Nkx2.2 binding sites within 10,000 bp of their gene loci that furthermore are differently expressed in absence or lower expression of Nkx2.2. Functionally, the target genes are associated with mitosis, migration stop, protein transport, lipid metabolism, mitochondrial biogenesis, formation of Ca2+ waves, and WNT signalling. Furthermore, motif discovery techniques and tests for overlaps between sequencing reads suggest that MYRF, OLIG2, SOX10, and TCF3 interact or compete with Nkx2.2 in OPCs/Ols. However, the activator versus repressor activity of Nkx2.2 does not seem to depend on the potential interaction with either of the transcription factors. Test for overlaps with sites of specific histone 3 modifications show that the Nkx2.2 binding sites are more frequently associated H3K4me3 and H3K27ac in genes to which Nkx2.2 may act as an activator. This supports previous studies showing that Nkx2.2 acts in a HDAC1 dependent way. Together this provides new insight into how Nkx2.2 contributes to the timing of OPC differentiation and myelination in CNS.

2019-11-01 | GSE73921 | GEO

Gene expression profiling of wild-type, Nkx2.2 null, NeuroD null and Nkx2.2/NeuroD double KO E13.5 pancreata

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Transcription profiling of mouse wild type and Nkx2.2 mutant embryos at E12.5 and E13.5 to identify a transcripional program that Nkx2.2 regulation in the pancreas

Project description:The goal of this experiment was to analyze expression changes in the pancreas at embryonic days 12.5 and 13.5 between wild type and Nkx2.2 null mice. We know that Nkx2.2 is essential for pancreatic endocrine differentiation and development. At these early time points which are critical for endocrine cell specification, we would like to identify a transcriptional program that Nkx2.2 regulates. We would also like to identify direct and functional transcriptional targets of Nkx2.2.

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

Genome-wide disclosure of the Nkx2.2 targets in oligodendrocytes and their progenitor cells suggests several novel target genes

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Genome-wide assessment of Nkx2.2 binding sites in MIN6 pancreatic beta cell line

Project description:Through ChIP-Seq analysis we found Nkx2.2 to bind to important beta cell genes as well as to non beta endocrine ones.

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WT vs Nkx2.2-/- (null) cells at E15.5

Project description:Whole transcriptome analysis of Ngn3-expressing cells in WT and Nkx2.2 Null mouse embryos.

2015-02-24 | E-MTAB-3357 | biostudies-arrayexpress

mRNAseq analysis of Nkx2.2, Nkx6.1, and Olig2 overexpression in neural progenitors

Project description:Nkx2.2, Nkx6.1, and Olig2 repressors were overexpressed, singly or in combination, in in vitro-derived mouse neural progenitors to identify thier repression targets Overexpression study to identify genes repressed by Nkx2.2, Nkx6.1, and Olig2 in neural progenitors

2015-08-24 | E-GEOD-65457 | biostudies-arrayexpress

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

Project description: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

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