p16INK4a induces an age-dependent decline in islet regenerative potential

Janakiraman Krishnamurthy, Matthew R. Ramsey, Keith L. Ligon, Chad Torrice, Angela Koh, Susan Bonner-Weir and Norman E. Sharpless ()
Additional contact information
Janakiraman Krishnamurthy: The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine
Matthew R. Ramsey: The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine
Keith L. Ligon: Brigham and Women's Hospital and Harvard Medical School
Chad Torrice: The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine
Angela Koh: Joslin Diabetes Center and Harvard Medical School
Susan Bonner-Weir: Joslin Diabetes Center and Harvard Medical School
Norman E. Sharpless: The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine

Nature, 2006, vol. 443, issue 7110, 453-457

Abstract: Stem cell ageing In this issue, three separate labs report the discovery of a protein that regulates ageing specifically in stem cells. This helps answer a fundamental question: why do mammalian progenitor cells gradually lose their ability to divide and generate new cells as they grow old? Norman Sharpless and colleagues generated a knockout mouse lacking tumour suppressor p16INK4a, a protein involved in cell cycle control and known to be expressed in an age-dependent manner. Studying its role in regeneration of the blood, pancreas and brain, the three groups separately found that p16INK4a is not only a biomarker, but an effector of ageing. By comparing the effect of elevated or reduced p16INK4a expression in mice, they found that p16INK4a halts proliferation of stem cells, but only in older mice. Taken together, the work suggests that p16INK4a reduces cancer incidence via its tumour suppressor action, at the same time contributing to ageing by reducing stem cell function. The work also suggests that type 2 diabetes might be linked to the failure of the pancreatic islets to renew, and that blocking this protein in certain tissues might combat some effects of ageing.

Date: 2006
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/nature05092 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:443:y:2006:i:7110:d:10.1038_nature05092

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature05092

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().