S6K in geroconversion
Markers of cellular senescence depend in part on the MTOR (mechanistic target of rapamycin) pathway. MTOR participates in geroconversion, a conversion from reversible cell cycle arrest to irreversible senescence. Recently we demonstrated that hyper-induction of cyclin D1 during geroconversion was mo...
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| Format: | Online |
| Language: | English |
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Landes Bioscience
2013
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3885635/ |
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pubmed-38856352014-01-10 S6K in geroconversion Leontieva, Olga V Demidenko, Zoya N Blagosklonny, Mikhail V Extra Views Markers of cellular senescence depend in part on the MTOR (mechanistic target of rapamycin) pathway. MTOR participates in geroconversion, a conversion from reversible cell cycle arrest to irreversible senescence. Recently we demonstrated that hyper-induction of cyclin D1 during geroconversion was mostly dependent on MEK, whereas rapamycin only partially inhibited cyclin D1 accumulation. Here we show that, while not affecting cyclin D1, siRNA for p70S6K partially prevented loss of RP (replicative/regenerative potential) during p21-induced cell cycle arrest. Similarly, an inhibitor of p70 S6 kinase (PF-4708671) partially inhibited phosphorylation of S6 and preserved RP, while only marginally prevented cyclin D1 induction. Thus S6K and MEK play different roles in geroconversion. Landes Bioscience 2013-10-15 2013-09-09 /pmc/articles/PMC3885635/ /pubmed/24036549 http://dx.doi.org/10.4161/cc.26248 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Leontieva, Olga V Demidenko, Zoya N Blagosklonny, Mikhail V |
| spellingShingle |
Leontieva, Olga V Demidenko, Zoya N Blagosklonny, Mikhail V S6K in geroconversion |
| author_facet |
Leontieva, Olga V Demidenko, Zoya N Blagosklonny, Mikhail V |
| author_sort |
Leontieva, Olga V |
| title |
S6K in geroconversion |
| title_short |
S6K in geroconversion |
| title_full |
S6K in geroconversion |
| title_fullStr |
S6K in geroconversion |
| title_full_unstemmed |
S6K in geroconversion |
| title_sort |
s6k in geroconversion |
| description |
Markers of cellular senescence depend in part on the MTOR (mechanistic target of rapamycin) pathway. MTOR participates in geroconversion, a conversion from reversible cell cycle arrest to irreversible senescence. Recently we demonstrated that hyper-induction of cyclin D1 during geroconversion was mostly dependent on MEK, whereas rapamycin only partially inhibited cyclin D1 accumulation. Here we show that, while not affecting cyclin D1, siRNA for p70S6K partially prevented loss of RP (replicative/regenerative potential) during p21-induced cell cycle arrest. Similarly, an inhibitor of p70 S6 kinase (PF-4708671) partially inhibited phosphorylation of S6 and preserved RP, while only marginally prevented cyclin D1 induction. Thus S6K and MEK play different roles in geroconversion. |
| publisher |
Landes Bioscience |
| publishDate |
2013 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3885635/ |
| _version_ |
1612045820609167360 |