Cited by 212Developmental Biology and Gene RegulationPancreatic function and diabetesCongenital heart defects research

Activin receptor patterning of foregut organogenesis

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Kim, Seung K., Hebrok, Matthias, Li, En, Oh, S. Paul, Schrewe, Heinrich, Harmon, Erin B., Lee, Joon S., Melton, Douglas A.·2000·Genes & Development

Abstract

Foregut development produces a characteristic sequence of gastrointestinal and respiratory organs, but the signaling pathways that ensure this developmental order remain largely unknown. Here, mutations of activin receptors ActRIIA and ActRIIB are shown to disrupt the development of posterior foregut-derived organs, including the stomach, pancreas, and spleen. Foregut expression of genes including Shh and Isl1 is shifted in mutant mice. The endocrine pancreas is particularly sensitive to the type and extent of receptor inactivation. ActRIIA+/−B+/−animals lack axial defects, but have hypoplastic pancreatic islets, hypoinsulinemia, and impaired glucose tolerance. Thus, activin receptor-mediated signaling regulates axial patterning, cell differentiation, and function of foregut-derived organs.

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Crossref · 10.1101/gad.14.15.1866

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  • FGF2 and Activin, secreted by the notochord, lead to expression of pancreatic markers by repressing Shh in pancreatic endoderm.

    “FGF2 and Activin, secreted by the notochord, lead to the expression of pancreatic markers by repressing expression of Shh in pancreatic endoderm [15-19].”

    From A systematic screen for genes expressed in definitive endoderm by Serial Analysis of Gene Expression (SAGE) (2007) · cites this paper as [17]

    The Results and Discussion say that notochord-derived activin signals may repress Shh in chick pancreatic endoderm, and report that activin receptor signaling restricts Shh in mouse foregut endoderm and regulates pancreatic Isl1 expression. They do not establish the claimed pathway from Shh repression to pancreatic-marker expression or address a role for FGF2. Page numbers are unavailable in our copy. (LLM, conf=0.86)

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Authors
Kim, S. K., Hebrok, M., Li, E., Oh, S. P., Schrewe, H., Harmon, E. B., Lee, J. S., & Melton, D. A.
Affiliations
Howard Hughes Medical Institute (US)
Venue
Genes & Development
Published
2000-08-01
Volume
14
Issue
15
Pages
1866-1871
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W1768073869
Cited by
212
References
33
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 6 · 2019: 3 · 2018: 9 · 2017: 5 · 2016: 5 · 2015: 8 · 2014: 8 · 2013: 8 · 2012: 10
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Howard Hughes Medical Institute
  • American Diabetes Association
  • Donald E. and Delia B. Baxter Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
Keywords
activin receptors, ActRIIA, ActRIIB, pancreatic islets, endocrine pancreas, hypoinsulinemia, glucose tolerance, stomach development, spleen development, Sonic hedgehog, Isl1, axial patterning, mouse mutants
MeSH terms
Animals, Cell Differentiation, Digestive System, Digestive System Physiological Phenomena, Glucose Tolerance Test, Hyperplasia, Insulin, Male, Mice, Mutant Strains, Nerve Tissue Proteins, Pancreas, Proteins, Spleen, Stomach, Transcription Factors, Trans-Activators, Receptors, Growth Factor, Homeodomain Proteins, Body Patterning, Activin Receptors, Type II, Mice, Hedgehog Proteins, LIM-Homeodomain Proteins

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