Genetic rescue of Cdk4 null mice restores pancreatic β-cell proliferation but not homeostatic cell number View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2003-08-14

AUTHORS

Javier Martín, Sarah L Hunt, Pierre Dubus, Rocío Sotillo, Fanny Néhmé-Pélluard, Mark A Magnuson, Albert F Parlow, Marcos Malumbres, Sagrario Ortega, Mariano Barbacid

ABSTRACT

Lack of Cdk4 expression in mice leads to insulin-deficient diabetes and female infertility owing to a reduced number of pancreatic β cells and prolactin-producing pituitary lactotrophs, respectively. Cdk4 null mice display also reduced body and organ size. Here, we show that Cdk4 is essential for the postnatal proliferation of pancreatic β cells but not for embryonic neogenesis from ductal epithelial cells. Re-expression of endogenous Cdk4 in β cells and in the pituitary gland of Cdk4 null mice restores cell proliferation and results in fertile and normoglycemic animals, thus, demonstrating that the proliferation defects in these cellular populations are cell autonomous because of the lack of Cdk4 expression. However, these mice remain small in size, indicating that this phenotype is not because of pancreatic- or pituitary-mediated endocrine defects. This phenotype is a consequence of reduced cell numbers rather than reduced cell size. Thus, mammalian Cdk4 is not only involved in controlling proliferation of specific cell types but may play a wider role in establishing homeostatic cell numbers. More... »

PAGES

5261-5269

References to SciGraph publications

  • 1995-03. Principles of CDK regulation in NATURE
  • 2001-12. To cycle or not to cycle: a critical decision in cancer in NATURE REVIEWS CANCER
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.onc.1206506

    DOI

    http://dx.doi.org/10.1038/sj.onc.1206506

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1014548918

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12917627


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