Genome-wide assessment of Nkx2.2 binding sites in MIN6 pancreatic beta cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE79785 | GEO | 2016/12/20
SECONDARY ACCESSION(S): PRJNA316994
REPOSITORIES: GEO
Similar Datasets
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
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
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
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
2016-12-20 | GSE79724 | GEO
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 | GSE273744 | GEO
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 | GSE273743 | GEO
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 | GSE273742 | GEO
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 | GSE273741 | GEO
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