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mRNA Decay Factor AUF1 Maintains Normal Aging, Telomere Maintenance, and Suppression of Senescence by Activation of Telomerase Transcription
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AUF1 is implicated in the cessation of the inflammatory response by mediating cytokine mRNA degradation.
“the mRNA decay factor AUF1, which is implicated in the cessation of the inflammatory response by mediating cytokine mRNA degradation”
From The Hallmarks of Aging (2013) · cites this paper as Pont et al., 2012
AUF1 contributes to maintaining telomere length by activating the expression of the telomerase catalytic subunit TERT.
“AUF1 contributes to maintaining telomere length by activating the expression of the telomerase catalytic subunit TERT”
From The Hallmarks of Aging (2013) · cites this paper as Pont et al., 2012
AUF1-deficient mice exhibit marked cellular senescence and a premature aging phenotype that can be rescued by re-expression of this RNA-binding factor.
“AUF1-deficient mice exhibit a marked cellular senescence and premature aging phenotype that can be rescued by re-expression of this RNA-binding factor”
From The Hallmarks of Aging (2013) · cites this paper as Pont et al., 2012
AUF1 deficiency accelerates ageing in mice and increases senescence in mouse and human cells.
“AUF1 deficiency accelerates ageing in mice and increases senescence in both mouse and human cells [15].”
From RNA binding protein AUF1/HNRNPD regulates nuclear export, stability and translation of SNCA transcripts (2023) · cites this paper as [15]
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Citations
Cites
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“…Phenotype While increased stabilization of cell-cycle checkpoint mRNAs promotes cellular senescence, it cannot account for the genetic anticipation phenotype, previously associated with telomere dysfunction in mice (Herrera et al., 1999; Rudolph et al., 1999; d’Adda di Fagagna et al., 2003).”
Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA
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“AUF1 Is Directly Responsible for the Genetic Anticipation Phenotype While increased stabilization of cell-cycle checkpoint mRNAs promotes cellular senescence, it cannot account for the genetic anticipation phenotype, previously associated with telomere dysfunction in mice (Herrera et al., 1999; Rudolph et al., 1999; d…”
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Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing
Molofsky, A. V., Slutsky, S. G., Joseph, N. M., He, S., Pardal, R., Krishnamurthy, J., Sharpless, N. E., & Morrison, S. J. (2006) · Nature · doi:10.1038/nature05091 · Cited by 972 · cited 2×
“, 2004), and increased p16 protein accumulation is associated with reduced cell and tissue viability (Krishnamurthy et al., 2004; Molofsky et al., 2006; Liu et al., 2011).”
Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice
Jaskelioff, M., Muller, F. L., Paik, J.-H., Thomas, E., Jiang, S., Adams, A. C., Sahin, E., Kost-Alimova, M., Protopopov, A., Cadiñanos, J., et al. (2011) · Nature · doi:10.1038/nature09603 · Cited by 857 · cited 2×
“Failure to maintain telomere integrity results in genomic instability; DNA damage responses, particularly at the ends of chromosomes; increased cellular senescence; and organ degeneration, which are key drivers of the natural aging process (De Lange, 2005; Jaskelioff et al., 2011; Sahin and Depinho, 2010).”
Linking functional decline of telomeres, mitochondria and stem cells during ageing
Sahin, E., & DePinho, R. A. (2010) · Nature · doi:10.1038/nature08982 · Cited by 759
Disease states associated with telomerase deficiency appear earlier in mice with short telomeres
Herrera, E., Samper, E., Martín‐Caballero, J., Flores, J. M., Lee, H., & Blasco, M. A. (1999) · The EMBO Journal · doi:10.1093/emboj/18.11.2950 · Cited by 471 · cited 4×
“with telomerase knockout mice (Herrera et al., 1999), there was a stronger phenotype and greater decrease in number and survival of Auf1 / offspring in a congenic C57BL/6 background (Figure S2D).”
InfluentialEffect of TERT over-expression on the long-term transplantation capacity of hematopoietic stem cells
Allsopp, R. C., Morin, G. B., Horner, J. W., DePinho, R., Harley, C. B., & Weissman, I. L. (2003) · Nature Medicine · doi:10.1038/nm0403-369 · Cited by 155
Expression of p16INK4a prevents cancer and promotes aging in lymphocytes
Liu, Y., Johnson, S. M., Fedoriw, Y., Rogers, A. B., Yuan, H., Krishnamurthy, J., & Sharpless, N. E. (2011) · Blood · doi:10.1182/blood-2010-09-304402 · Cited by 114
Telomeres and immunological diseases of aging.
Andrews, N. P., Fujii, H., Goronzy, J. J., & Weyand, C. M. (2010) · Gerontology · doi:10.1159/000268620 · Cited by 108
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Aging Hallmarks: The Benefits of Physical Exercise
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BackgroundNF90 coordinately represses the senescence-associated secretory phenotype
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Metadata
- Authors
- Pont, A. R., Sadri, N., Hsiao, S. J., Smith, S., & Schneider, R. J.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2012-07
- Volume
- 47
- Issue
- 1
- Pages
- 5-15
- ISSN
- 1097-2765
- PMC
- PMC3966316
- Cited by
- 139
- References
- 12
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 417 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Funders
- National Institutes of Health (GM R01 GM085693-03, T32 T32AI007180)
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