Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA939831 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23649130.fastq.gz	Fastqsanger.gz
	SRR23649131.fastq.gz	Fastqsanger.gz
	SRR23649132.fastq.gz	Fastqsanger.gz
	SRR23649133.fastq.gz	Fastqsanger.gz
	SRR23649134.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

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

Functional analysis of the Nkx2.2 SD domain: gene expression profiling of E16.5 Nkx2.2 SD mutant pancreata versus wild-type littermate pancreata

Project description:The experiment consists of 7 one channel assays for analyzing embryonic pancreas at E16.5. There are three or four replicates per condition. At E16.5, we are looking at differential gene expression across two mouse lines, WT vs Nkx2.2 SD mutants.

2015-01-29 | E-MTAB-3349 | biostudies-arrayexpress

RNAseq analysis of the duodenum of intestine-specific adult SD mutant mice

Project description:Aim: Transcriptional analysis of the duodenum of adult Nkx2.2flox/SD;Villin-Cre (SDint) 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: 206 genes with a p-value <0.05 were significantly changed. Among these are some enteroendocrine hormones. Conclusion: The SD domain of Nkx2.2 regulates specification of some enteroendocrine cells

2016-07-28 | GSE72762 | GEO

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

RNAseq analysis of the duodenum of intestine-specific adult SD mutant mice

2016-07-28 | E-GEOD-72762 | biostudies-arrayexpress

NKX2.2

Project description:NKX2.2

| PRJNA316849 | ENA

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

Project description:Aim: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

2016-12-20 | GSE79723 | GEO

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

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

Project description:The experiment consist of 16 one channel assays for analyzing embryonic pancreas at E13. There are four replicates per condition. We are looking at differential gene expression across four mouse lines: WT, Nkx2.2, NeuroD and Nkx2.2/NeuroD double mutants at E13.5.

2015-02-03 | E-MTAB-3350 | biostudies-arrayexpress

NKX2.2 and KLF4 cooperate to regulate α cell identity [islet_alpha_klf4_KO_RNAseq]

Project description:Transcription factors (TF) are indispensable for maintaining cell identity through regulating cell specific gene expression. Distinct cell identities derived from a common progenitor are frequently perpetuated by shared TFs; yet the mechanisms that facilitate their cell specific regulatory targets are poorly characterized. We report that the TF NKX2.2 is critical for the identity of pancreatic islet α cells by directly activating α cell genes and repressing alternate islet cell fate genes. When compared to the known role of NKX2.2 in islet β cells, we demonstrate that NKX2.2 regulates novel α cell target genes, facilitated in part by α cell specific DNA binding at gene promoters. Furthermore, we have identified the reprogramming factor KLF4 as having enriched expression in α cells, where it co-occupies NKX2.2-bound α cell promoters and is necessary for NKX2.2 binding in α cells to co-regulate many NKX2.2 α cell transcriptional targets. Misexpression of Klf4 in β cells is sufficient to manipulate chromatin accessibility, increase binding of NKX2.2 at α cell specific promoters sites, and alter expression of NKX2.2-regulated cell specific targets. This study identifies KLF4 is a novel α cell identity factor that cooperates with NKX2.2 to regulate α cell identity.

2025-02-12 | GSE273740 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data