Zobrazeno 1 - 10
of 56
pro vyhledávání: '"Olga V Leontieva"'
Autor:
Alexandra V. Vylegzhanina, Ivan A. Bespalov, Ksenia A. Novototskaya-Vlasova, Brandon M. Hall, Anatoli S. Gleiberman, Han Yu, Olga V. Leontieva, Katerina I. Leonova, Oleg V. Kurnasov, Andrei L. Osterman, Grace K. Dy, Alexey A. Komissarov, Elena Vasilieva, Jeff Gehlhausen, Akiko Iwasaki, Christine B. Ambrosone, Takemasa Tsuji, Junko Matsuzaki, Kunle Odunsi, Ekaterina L. Andrianova, Andrei V. Gudkov
LINE-1 (L1), the most abundant family of autonomous retrotransposons occupying over 17% of human DNA, is epigenetically silenced in normal tissues but frequently derepressed in cancer, suggesting that L1-encoded proteins may act as tumor-associated a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::8477abcfdeea873bdfbc1aaddff4cbf4
https://doi.org/10.1101/2023.02.03.526997
https://doi.org/10.1101/2023.02.03.526997
Autor:
David Frescas, Evguenia Strom, Tamara Tchkonia, Valeria Kogan, Brandon M. Hall, Slavoljub Vujcic, Yi Zhu, Peter Krasnov, James L. Kirkland, Olga B. Chernova, Igor Koman, Marina P. Antoch, Andrei V. Gudkov, Olga V. Leontieva, Anatoli S. Gleiberman
Publikováno v:
Aging Cell
Adipose tissue is recognized as a major source of systemic inflammation with age, driving age‐related tissue dysfunction and pathogenesis. Macrophages (Mφ) are central to these changes yet adipose tissue Mφ (ATMs) from aged mice remain poorly cha
Publikováno v:
PLoS ONE, Vol 6, Iss 10, p e26126 (2011)
Depending on cellular context, p53-inducing agents (such as nutlin-3a) cause different outcomes including reversible quiescence and irreversible senescence. Inhibition of mTOR shifts the balance from senescence to quiescence. In cell lines with incom
Externí odkaz:
https://doaj.org/article/c61d0441bed246a68b901ab5934810d2
Publikováno v:
Oncotarget
// Olga V. Leontieva 1 and Mikhail V. Blagosklonny 1 1 Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA Correspondence to: Mikhail V. Blagosklonny, email: // Olga V. Leontieva, email: // Keywords : mTORC1, rapalogs, sirolimus, agi
Publikováno v:
Aging (Albany NY)
Rapamycin slows organismal aging and delays age-related diseases, extending lifespan in numerous species. In cells, rapamycin and other rapalogs such as everolimus suppress geroconversion from quiescence to senescence. Rapamycin inhibits some, but no
Publikováno v:
Oncotarget
Phorbol ester (PMA or TPA), a tumor promoter, can cause either proliferation or cell cycle arrest, depending on cellular context. For example, in SKBr3 breast cancer cells, PMA hyper-activates the MEK/MAPK pathway, thus inducing p21 and cell cycle ar
Publikováno v:
Cell Cycle. 13:2656-2659
TOR is involved in aging in a wide range of species from yeast to mammals. Here we show that, after overnight fasting, mTOR activity is higher in the livers of 28 months old female mice compared with middle-aged mice. Taken together with previous rep
Publikováno v:
Cell Cycle
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-i
Publikováno v:
Cell Cycle
When the cell cycle is arrested, even though growth-promoting pathways such as mTOR are still active, then cells senesce. For example, induction of either p21 or p16 arrests the cell cycle without inhibiting mTOR, which, in turn, converts p21/p16-ind
Autor:
Zoya N. Demidenko, Mikhail A. Nikiforov, Olga V. Leontieva, A. E. Berman, James A. McCubrey, Venkatesh Natarajan
Publikováno v:
Oncotarget
It is widely believed that aging results from the accumulation of molecular damage, including damage of DNA and mitochondria and accumulation of molecular garbage both inside and outside of the cell. Recently, this paradigm is being replaced by the "