Requirement of Math1 for Secretory Cell Lineage Commitment in the Mouse Intestine
By Qi Yang, N. Bermingham, M. Finegold, H. Zoghbi. Science, 2001
976 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/47261095e58a0d8360113a21b934156a999a2a57
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Citations in the corpus
- Wnt signaling in the intestinal epithelium: from endoderm to cancer. (2005, background): “Accordingly, MATH1 deficient mice lack goblet, enteroendocrine, and Paneth cells but do produce enterocytes (Yang et al. 2001).”
- The intestinal crypt, a prototype stem cell compartment. (2013, background): “Conversely, Math1 deletion results in a complete loss of all secretory lineages (Shroyer et al., 2007; Yang et al., 2001), whereasMath1 overexpression is sufficient to direct progenitors into the secretory lineage (VanDussen and Samuel- 278 Cell 154, July 18, 2013 ª2013 Elsevier Inc. son, 2010).”
- The Hes gene family: repressors and oscillators that orchestrate embryogenesis (2007, background): “…of goblet, enteroendocrine and Paneth cells, whereas the activation of Notch-Hes1 signaling represses Math1, and thereby inhibits the generation of Math1-dependent cells (Jensen et al., 2000; Yang et al., 2001; Suzuki et al., 2005; van Es et al., 2005; Fre et al., 2005; Stanger et al., 2005).”
- 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): “In contrast to Hes1, loss of Math1 depletes secretory lineage cells (Yang et al., 2001).”
- Canonical Wnt signals are essential for homeostasis of the intestinal epithelium. (2003, background): “We tentatively concluded that the Wnt/ -catenin pathway is essential for the maintenance of Math1-positive progenitors for the secretory cell lineage.”
- Intestinal Goblet Cells and Mucins in Health and Disease: Recent Insights and Progress (2010, background): “Activation of Hath1 caused induction of MUC2, a major goblet cell mucin, by binding to its binding sites, Eboxes on MUC2 promoter [12, 13].”
- Epithelial stem cells: turning over new leaves. (2007, positive): “…neuroendocrine cells, Paneth cells, and goblet cells at the expense of intestinal enterocytes (Jensen et al., 2000; Suzuki et al., 2005) whereas the knockout of Math1 or gain-of-function mutations in Notch leads to the opposite phenotype (Fre et al., 2005; Stanger et al., 2005; Yang et al., 2001).”