p16INK4a induces an age-dependent decline in islet regenerative potential
By J. Krishnamurthy, M. R. Ramsey, K. Ligon, C. Torrice, A. Koh, S. Bonner-Weir, N. Sharpless. Nature, 2006
1,031 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/ae05049b3693e5d602dd7ff82ef78895c0f71a4b
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Citations in the corpus
- FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis (2009, background): “, p16) that appear to suppress cancer at the cost of tissue-resident stem cells and therefore may contribute to decreased regenerative potential during the aging process (Krishnamurthy et al., 2006; Molofsky et al., 2006).”
- Epigenetics: A Molecular Link Between Environmental Factors and Type 2 Diabetes (2009, background): “In support of this, an increased expression of Ink4a/Arf (Cdkn2a locus) was associated with reduced -cell regeneration in aging mice (82).”
- Mechanisms of stem cell self-renewal. (2009, background): “…activities and leading to cancer. overexpression of p15Ink4b/p16Ink4a/p19Arf and p53 increases mouse life span (Matheu et al. 2007), even though loss of p16Ink4a increases stem cell function in multiple tissues during aging ( Janzen et al. 2006, Krishnamurthy et al. 2006, Molofsky et al. 2006).”
- Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “Surprisingly, although p16INK4a expression drove a decline in β cell regenerative capacity and predisposed mice to mild diabetes (Krishnamurthy et al., 2006; Chen et al., 2009), senescent β islets increased insulin secretion, making it unclear how senescence contributes to maintain glucose homeostas”
- The biology of cancer stem cells. (2007, background): “Recent studies showed that p16 Ink4a plays a role in stem cell senescence in the blood, brain, and pancreatic islet cells ( Janzen et al. 2006, Krishnamurthy et al. 2006, Molofsky et al. 2006).”