Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing
By A. Molofsky, S. G. Slutsky, N. Joseph, Shenghui He, R. Pardal, J. Krishnamurthy, N. Sharpless, S. Morrison. Nature, 2006
991 citations recorded by the source corpus.
Subfields: Developmental Neuroscience, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/82e3e3c2598c2c7646e94ca76d07fb99fc419141
How researchers see this paper
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In Developmental Neuroscience
- Fred H. Gage
- Arturo Alvarez-Buylla
- Wei Deng
- Hongjun Song
- Guo-li Ming
- F. Doetsch
- Chunmei Zhao
- Rebecca A. Ihrie
In Molecular Biology
- J. Campisi
- S. Morrison
- K. Helin
- David M. Sabatini
- Arturo Alvarez-Buylla
- S. Baylin
- Manuel Serrano
- Peter A. Jones
In Physiology
- J. Campisi
- Jesús Gil
- Manuel Serrano
- R. DePinho
- Domhnall McHugh
- Guido Kroemer
- T. Arumugam
- N. Sharpless
Citations in the corpus
- Mechanisms and functional implications of adult neurogenesis. (2008, positive): “Studies with neurosphere cultures suggest that the self-renewal capacity and the number of SVZ progenitors decrease significantly in aged animals (Molofsky et al., 2006).”
- Senescence and the SASP: many therapeutic avenues (2020, background): “In response to tissue damage, the SASP can also promote cellular reprogramming in neighboring cells (Mosteiro et al. 2016) while reinforcing plasticity and stemness (Ritschka et al. 2017).”
- Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “This is marked by a twofold reduction in NSC numbers and a decreased proliferation, which correlates with increased expression of senescence markers in the regions where NSCs reside (Molofsky et al., 2006).”
- Four faces of cellular senescence (2011, positive): “, 2009), and its activity has been functionally linked to the reduction in progenitor cell number that occurs in multiple tissues during aging (Janzen et al., 2006; Krishnamurthy et al., 2006; Molofsky et al., 2006).”
- Stems cells and the pathways to aging and cancer. (2008, background): “, 2006), correlating with the diminished neurogenesis observed in the olfactory bulb of old mice (Molofsky et al., 2006).”
- Hmga2 promotes neural stem cell self-renewal in young, but not old, mice by reducing p16Ink4a and p19Arf expression (2008, background): “However, neural stem cell frequency, self-renewal capacity, and mitotic activity all decline with age along with the rate of neurogenesis (Enwere et al., 2004; Maslov et al., 2004; Molofsky et al., 2006).”
- A Specialized Vascular Niche for Adult Neural Stem Cells (2008, background): “, 1981) may underlie age-dependent decline of SVZ function (Luo et al., 2006; Molofsky et al., 2006; Tanaka et al., 2007).”
- mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “For instance, the cell cycle regulators p16 (also known as INK4a) and p19 (also known as ARF) act as a brake to limit the proliferation of the stem cell pool, but their age-dependent accumulation ultimately causes stem cells to undergo senescence”
- The hallmarks of aging. (2013, background): “A similar functional attrition of stem cells has been found in essentially all adult stem cell compartments, including the mouse forebrain (Molofsky et al., 2006), the bone (Gruber et al.”
- Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “Consistent with its role as an important glioma tumor suppressor, p16 Ink4a is also a critical inhibitor of progenitor cell renewal in the sub-ventricular zone of aging mice (Molofsky et al. 2006).”
- Lake-front property: a unique germinal niche by the lateral ventricles of the adult brain. (2011, positive): “The expression of epigenetic regulators like Bmi-1 is altered as the organism ages and stem cell function declines (Molofsky et al., 2003; Molofsky et al., 2006; Fasano et al., 2009).”