ArticleDevelopmental biology2011
Nkx2.2 and Arx genetically interact to regulate pancreatic endocrine cell development and endocrine hormone expression.
Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- NKX2.2 and KLF4 cooperate to regulate α-cell identity.Genes & development · 2025Article
- Inferring regulators of cell identity in the human adult pancreas.NAR genomics and bioinformatics · 2023Article
- Not the second fiddle: α cell development, identity, and function in health and diabetes.The Journal of endocrinology · 2023Review
- Exploring the Effects of Metabolism-Disrupting Chemicals on Pancreatic α-Cell Viability, Gene Expression and Function: A Screening Testing Approach.International journal of molecular sciences · 2023Article
- EpiCRISPR targeted methylation of Arx gene initiates transient switch of mouse pancreatic alpha to insulin-producing cells.Frontiers in endocrinology · 2023Article
- NEUROD1 Is Required for the Early α and β Endocrine Differentiation in the Pancreas.International journal of molecular sciences · 2021Article
- Differential Morphological Diagnosis of Various Forms of Congenital Hyperinsulinism in Children.Frontiers in endocrinology · 2021Article
- Development and Characteristics of Pancreatic Epsilon Cells.International journal of molecular sciences · 2019Review
- Neurog3-Independent Methylation Is the Earliest Detectable Mark Distinguishing Pancreatic Progenitor Identity.Developmental cell · 2019Article
- Gene Signature of the Human Pancreatic ε Cell.Endocrinology · 2018Article
- NKX2.2, PDX-1 and CDX-2 as potential biomarkers to differentiate well-differentiated neuroendocrine tumors.Biomarker research · 2018Article
- Loss of mTORC1 signaling alters pancreatic α cell mass and impairs glucagon secretion.The Journal of clinical investigation · 2017Article
- Converting Adult Pancreatic Islet α Cells into β Cells by Targeting Both Dnmt1 and Arx.Cell metabolism · 2017Article
- Article
- Pancreatic β cell identity requires continual repression of non-β cell programs.The Journal of clinical investigation · 2017Article
- Generation of a Conditional Allele of the Transcription Factor Atonal Homolog 8 (Atoh8).PloS one · 2016Article
- Transcription factor regulation of pancreatic organogenesis, differentiation and maturation.Islets · 2016Review
- Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells.Development (Cambridge, England) · 2015Article
- Glucagon is essential for alpha cell transdifferentiation and beta cell neogenesis.Development (Cambridge, England) · 2015Article
- Role of transcription factors in the transdifferentiation of pancreatic islet cells.Journal of molecular endocrinology · 2015Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Nkx2.2 and Arx are essential pancreatic transcription factors. Nkx2.2 is necessary for the appropriate specification of the islet alpha, beta, PP and epsilon cell lineages, whereas Arx is required to form the correct ratio of alpha, beta, delta and PP cells. To begin to understand the cooperative functions of Nkx2.2 and Arx in the development of endocrine cell lineages, we generated progenitor cell-specific deletions of Arx on the Nkx2.2 null background. The analysis of these mutants demonstrates that expansion of the ghrelin cell population in the Nkx2.2 null pancreas is not dependent on Arx; however, Arx is necessary for the upregulation of ghrelin mRNA levels in Nkx2.2 mutant epsilon cells. Alternatively, in the absence of Arx, delta cell numbers are increased and Nkx2.2 becomes essential for the repression of somatostatin gene expression. Interestingly, the dysregulation of ghrelin and somatostatin expression in the Nkx2.2/Arx compound mutant (Nkx2.2(null);Arx(Δpanc)) results in the appearance of ghrelin+/somatostatin+ co-expressing cells. These compound mutants also revealed a genetic interaction between Nkx2.2 and Arx in the regulation of the PP cell lineage; the PP cell population is reduced when Nkx2.2 is deleted but is restored back to wildtype numbers in the Nkx2.2(null);Arx(Δpanc) mutant. Moreover, conditional deletion of Arx in specific pancreatic cell populations established that the functions of Arx are necessary in the Neurog3+ endocrine progenitors. Together, these experiments identify novel genetic interactions between Nkx2.2 and Arx within the endocrine progenitor cells that ensure the correct specification and regulation of endocrine hormone-producing cells.
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