Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
about
The inactivation of Arx in pancreatic α-cells triggers their neogenesis and conversion into functional β-like cellsIncomplete Re-Expression of Neuroendocrine Progenitor/Stem Cell Markers is a Key Feature of β-Cell Dedifferentiation.Pharmacological induction of pancreatic islet cell transdifferentiation: relevance to type I diabetesβ-Cell Replacement Strategies: The Increasing Need for a "β-Cell Dogma".Islet-1 Is essential for pancreatic β-cell function.Transdifferentiation of pancreatic α-cells into insulin-secreting cells: From experimental models to underlying mechanisms.Dysgenesis of enteroendocrine cells in Aristaless-Related Homeobox polyalanine expansion mutations.Limited impact on glucose homeostasis of leptin receptor deletion from insulin- or proglucagon-expressing cellsThe FOXP1, FOXP2 and FOXP4 transcription factors are required for islet alpha cell proliferation and function in mice.Early pancreatic islet fate and maturation is controlled through RBP-JκArx polyalanine expansion in mice leads to reduced pancreatic α-cell specification and increased α-cell death.PAR2 regulates regeneration, transdifferentiation, and deathPdx1 maintains β cell identity and function by repressing an α cell program.Grg3/TLE3 and Grg1/TLE1 induce monohormonal pancreatic β-cells while repressing α-cell functions.The regulation of pre- and post-maturational plasticity of mammalian islet cell mass.Insulin-like genes in ascidians: findings in Ciona and hypotheses on the evolutionary origins of the pancreasRole of transcription factors in the transdifferentiation of pancreatic islet cells.Evolving function and potential of pancreatic alpha cells.β-cell differentiation status in type 2 diabetes.Epigenetics in formation, function, and failure of the endocrine pancreas.Plasticity and dedifferentiation within the pancreas: development, homeostasis, and disease.Artemether Does Not Turn α Cells into β Cells.Epileptic Encephalopathies as Neurodegenerative Disorders.Distinct roles for the mTOR pathway in postnatal morphogenesis, maturation and function of pancreatic islets.Converting Adult Pancreatic Islet α Cells into β Cells by Targeting Both Dnmt1 and Arx.Partial ablation of leptin signaling in mouse pancreatic α-cells does not alter either glucose or lipid homeostasis.SIRT1 activation attenuates α cell hyperplasia, hyperglucagonaemia and hyperglycaemia in STZ-diabetic mice
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P2860
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
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2013 nî lūn-bûn
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2013 թուականին հրատարակուած գիտական յօդուած
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2013 թվականին հրատարակված գիտական հոդված
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2013年の論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年论文
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name
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@ast
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@en
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@nl
type
label
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@ast
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@en
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@nl
prefLabel
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@ast
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@en
Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@nl
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P2860
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Pancreatic α-cell specific deletion of mouse Arx leads to α-cell identity loss
@en
P2093
Catherine Lee May
Crystal L Wilcox
Erik R Walp
Natalie A Terry
Randall A Lee
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P304
P3181
P356
10.1371/JOURNAL.PONE.0066214
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P577
2013-01-01T00:00:00Z