Direct evidence for the pancreatic lineage: NGN3+ cells are islet progenitors and are distinct from duct progenitors.

By Guoqiang Gu, Jolanta Dubauskaite, D. Melton. Development, 2002

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View Paper: https://www.semanticscholar.org/paper/20694b9c75d8e0869274b949b22740c518e6772b

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Citations in the corpus

• Opposing actions of Arx and Pax4 in endocrine pancreas development. (2003, methodology): “GENES & DEVELOPMENT 17:2591–2603 © 2003 by Cold Spring Harbor Laboratory Press ISSN 0890-9369/03 $5.00; www.genesdev.org 2591 further demonstrated by lineage studies using the Cre/ LoxP system (Gu et al. 2002).”
• Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, methodology): “To express the Kras allele and to delete both copies of the conditional Ink4a/Arf allele specifically in the pancreas, we used the Pdx1-Cre transgene, shown previously to delete efficiently loxPcontaining alleles in all pancreatic lineages (endocrine, exocrine, and duct cells; Gu et al. 2002).”
• β Cells Can Be Generated from Endogenous Progenitors in Injured Adult Mouse Pancreas (2008, background): “, 2000) and extremely rare in normal postnatal pancreas (Gu et al., 2002).”
• Pancreatic β-Cell Dedifferentiation As Mechanism Of Diabetic β-Cell Failure (2012, unknown): “Mice Ins2-cre (Herrera, 2000), Rosa26-eGfp (Gu et al., 2002), InsR (Accili et al.”
• Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer. (2006, methodology): “We crossed Smad4 homozygous mice to either the Pdx1-Cre or Ptf1a-Cre transgenic mice (Gu et al. 2002; Kawaguchi et al. 2002) (hereafter, for brevity, Cre will be used for references to both strains together); these transgenes direct Cre recombinase expression to the epithelial lineages of the embryo”
• Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer (2010, methodology): “As the frequency of Cre-mediated recombination should be much higher using the Pdx1-driven Cre recombinase (21); and, given that the majority of recombined Kras-expressing cells were selectively lost from the pancreas, we hypothesized that the mutant Kras-expressing cells that persisted were derived”
• Pancreas organogenesis: From bud to plexus to gland (2011, background): “Recent clonal analysis by Degraz et al. (2009) further revealed that the majority of the Ngn3HI endocrine progenitors are individually unipotent and mitotically quiescent, a conclusion in accordance with previous studies (Gu et al., 2002).”
• In vivo derivation of glucose-competent pancreatic endocrine cells from bone marrow without evidence of cell fusion. (2003, background): “Alternatively, these cells may enter an intermediary pool of one (43) or more multipotent cell phenotype(s) within the endocrine or nonendocrine compartments of the pancreas or as oval cells within the liver (15).”
• Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “Pdx1 is required for further pancreatic development (Ohlsson et al. 1993; Offield et al. 1996), and its expression in all progenitor cells has made the Pdx1 promoter a useful tool for directing transgene expression during the bud stage (Gu et al. 2002) (see mouse models below).”