Control of endodermal endocrine development by Hes-1

By Jan Jensen, E. E. Pedersen, P. Galante, Jacob Hald, R. S. Heller, Makoto Ishibashi, Ryoichiro Kageyama, François Guillemot, P. Serup, O. Madsen. Nature Genetics, 2000

1,222 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/99c4e900f814e33a486e2cc11be45ed36fcb125a

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Citations in the corpus

• The Hes gene family: repressors and oscillators that orchestrate embryogenesis (2007, background): “Inactivation of Hes1 in mice leads to the upregulation of Ngn3, an acceleration of post-mitotic endocrine cell differentiation and severe pancreatic hypoplasia (Jensen et al., 2000).”
• Modulation of notch processing by gamma-secretase inhibitors causes intestinal goblet cell metaplasia and induction of genes known to specify gut secretory lineage differentiation. (2004, background): “…relate to chronic dysregulation of elements in the Notch pathway in a pattern similar to that observed in developing embryos with Hes1 deletions (Jensen et al., 2000 .9-fold, 9.1-fold, and 6.0-fold, respectively, that of vehicle controls by day 3, dipping slightly as crypt enterocyte…”
• Organogenesis and development of the liver. (2010, background): “The expression of SOX17 is controlled by homolog of hairy/enhancer-of-split (Hes-1): in the absence of Hes-1 the mice not only display accelerated differentiation of pancreatic endocrine cells from pancreatic progenitors (Jensen et al., 2000), the bile duct cells also differentiate to a pancreatic p”
• Wnt signaling in the intestinal epithelium: from endoderm to cancer. (2005, background): “1999), while Hes1 transcriptionally represses MATH1 expression (Jensen et al. 2000; Zheng et al. 2000).”
• Epithelial stem cells: turning over new leaves. (2007, neutral): “tinal enterocytes (Jensen et al., 2000; Suzuki et al., 2005) whereas the knockout of Math1 or gain-of-func-”
• Mammalian Krüppel-Like Factors in Health and Diseases (2010, background): “An additional mechanism by which KLF4 suppresses intestinal tumor formation involves Notch signaling, which suppresses goblet cell differentiation in the intestinal epithelium and is upregulated in intestinal tumors (197, 430).”
• Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. (2003, background): “Although apparently necessary for the early development of the pancreas, Notch signaling is normally suppressed in the adult organ (Apelqvist et al., 1999; Jensen et al., 2000).”
• Genetics and biology of pancreatic ductal adenocarcinoma. (2006, neutral): “1999; Jensen et al. 2000; Moshous et al. 2001; Hald et al. 2003; Murtaugh et al. 2003).”
• Pancreas organogenesis: From bud to plexus to gland (2011, background): “Consistent with this notion, Notch3 and Notch4 are expressed in the pancreatic mesenchyme during pancreas budding (Lammert et al., 2000; Jensen et al., 2000b).”
• The intestinal crypt, a prototype stem cell compartment. (2013, background): “What is the evidence for this? Deletion of Hes1 results in increased numbers of cells of all secretory lineages and decreased numbers of enterocytes (Jensen et al., 2000).”