Literature DB >> 23296649

Senescence regulation by mTOR.

Vjekoslav Dulic1.   

Abstract

The senescence program is activated in response to diverse stress stimuli potentially compromising genetic stability and leads to an irreversible cell cycle arrest. The mTOR pathway plays a crucial role in the regulation of cell metabolism and cellular growth. The goal of this chapter is to present evidence linking these two processes, which have one common regulator-the tumor suppressor p53. While the role of mTOR in senescence is still controversial, recent papers have shed new light onto this issue. This review, far from being exhaustive given the complexity of the field, will hopefully stimulate further research in this domain, whose relevance for ageing is becoming increasingly documented.

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Year:  2013        PMID: 23296649     DOI: 10.1007/978-1-62703-239-1_2

Source DB:  PubMed          Journal:  Methods Mol Biol        ISSN: 1064-3745


  23 in total

1.  Fasting levels of hepatic p-S6 are increased in old mice.

Authors:  Olga V Leontieva; Geraldine M Paszkiewicz; Mikhail V Blagosklonny
Journal:  Cell Cycle       Date:  2014       Impact factor: 4.534

Review 2.  Geroconversion: irreversible step to cellular senescence.

Authors:  Mikhail V Blagosklonny
Journal:  Cell Cycle       Date:  2014       Impact factor: 4.534

Review 3.  Senescence from G2 arrest, revisited.

Authors:  Véronique Gire; Vjekoslav Dulic
Journal:  Cell Cycle       Date:  2015       Impact factor: 4.534

4.  Cellular senescence and autophagy of myoepithelial cells are involved in the progression of in situ areas of carcinoma ex-pleomorphic adenoma to invasive carcinoma. An in vitro model.

Authors:  Carolina Amália Barcellos Silva; Elizabeth Ferreira Martinez; Ana Paula Dias Demasi; Albina Altemani; Jeruza Pinheiro da Silveira Bossonaro; Ney Soares Araújo; Vera Cavalcanti de Araújo
Journal:  J Cell Commun Signal       Date:  2015-04-21       Impact factor: 5.782

5.  Cellular senescence or EGFR signaling induces Interleukin 6 (IL-6) receptor expression controlled by mammalian target of rapamycin (mTOR).

Authors:  Christoph Garbers; Fabian Kuck; Samadhi Aparicio-Siegmund; Kirstin Konzak; Mareike Kessenbrock; Annika Sommerfeld; Dieter Häussinger; Philipp A Lang; Dirk Brenner; Tak W Mak; Stefan Rose-John; Frank Essmann; Klaus Schulze-Osthoff; Roland P Piekorz; Jürgen Scheller
Journal:  Cell Cycle       Date:  2013-09-18       Impact factor: 4.534

6.  Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program.

Authors:  Olga V Leontieva; Zoya N Demidenko; Mikhail V Blagosklonny
Journal:  Proc Natl Acad Sci U S A       Date:  2014-06-02       Impact factor: 11.205

Review 7.  Cellular senescence and its role in white adipose tissue.

Authors:  Ulf Smith; Qian Li; Mikael Rydén; Kirsty L Spalding
Journal:  Int J Obes (Lond)       Date:  2021-01-28       Impact factor: 5.095

8.  Dual mTORC1/C2 inhibitors suppress cellular geroconversion (a senescence program).

Authors:  Olga V Leontieva; Zoya N Demidenko; Mikhail V Blagosklonny
Journal:  Oncotarget       Date:  2015-09-15

Review 9.  mTOR Inhibition: From Aging to Autism and Beyond.

Authors:  Matt Kaeberlein
Journal:  Scientifica (Cairo)       Date:  2013-11-26

Review 10.  Cross-talk between HIF and p53 as mediators of molecular responses to physiological and genotoxic stresses.

Authors:  Joanna Obacz; Silvia Pastorekova; Borek Vojtesek; Roman Hrstka
Journal:  Mol Cancer       Date:  2013-08-14       Impact factor: 27.401

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