Search Results - "Leontieva, Olga V"

Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program by Leontieva, Olga V., Demidenko, Zoya N., Blagosklonny, Mikhail V.

“…During cell cycle arrest caused by contact inhibition (CI), cells do not undergo senescence, thus resuming proliferation after replating. The mechanism of…”
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CDK4/6-inhibiting drug substitutes for p21 and p16 in senescence: Duration of cell cycle arrest and MTOR activity determine geroconversion by Leontieva, Olga V., Blagosklonny, Mikhail V.

“…CDKN1A (p21) and CDKN2A (p16) inhibit CDK4/6, initiating senescence. According to our view on senescence, the role of p21 and p16 is to cause cell cycle…”
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Hypoxia suppresses conversion from proliferative arrest to cellular senescence by Leontieva, Olga V, Natarajan, Venkatesh, Demidenko, Zoya N, Burdelya, Lyudmila G, Gudkov, Andrei V, Blagosklonny, Mikhail V

“…Unlike reversible quiescence, cellular senescence is characterized by a large flat cell morphology, β-gal staining and irreversible loss of regenerative (i.e.,…”
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Weak p53 permits senescence during cell cycle arrest by Leontieva, Olga V., Gudkov, Andrei V., Blagosklonny, Mikhail V

“…Cell cycle arrest coupled with hyper-active mTOR leads to cellular senescence. While arresting cell cycle, high levels of p53 can inhibit mTOR (in some cell…”
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M(o)TOR of pseudo-hypoxic state in aging: Rapamycin to the rescue by Leontieva, Olga V., Blagosklonny, Mikhail V

“…A groundbreaking publication by Sinclair and coworkers has illuminated the pseudo-hypoxic state in aging and its reversibility. Remarkably, these data also fit…”
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The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway by Korotchkina, Lioubov G, Leontieva, Olga V, Bukreeva, Elena I, Demidenko, Zoya N, Gudkov, Andrei V, Blagosklonny, Mikhail V

“…Transient induction of p53 can cause reversible quiescence and irreversible senescence. Using nutlin-3a (a small molecule that activates p53 without causing…”
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Exploring long-term protection of normal human fibroblasts and epithelial cells from chemotherapy in cell culture by Apontes, Pasha, Leontieva, Olga V, Demidenko, Zoya N, Li, Fengzhi, Blagosklonny, Mikhail V

“…Killing of proliferating normal cells limits chemotherapy of cancer. Several strategies to selectively protect normal cells were previously suggested. Here we…”
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Suppression of replicative senescence by rapamycin in rodent embryonic cells by Pospelova, Tatyana V., Leontieva, Olga V., Bykova, Tatiana V., Zubova, Svetlana G., Pospelov, Valery A., Blagosklonny, Mikhail V.

“…The TOR (target of rapamycin) pathway is involved in aging in diverse organisms from yeast to mammals. We have previously demonstrated in human and rodent…”
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Hypoxia and gerosuppression: The mTOR saga continues by Leontieva, Olga V., Blagosklonny, Mikhail V

“…Growth-promoting and nutrient/mitogen-sensing pathways such as mTOR convert p21- and p16-induced arrest into senescence (geroconversion). We have recently…”
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Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin by Leontieva, Olga V, Demidenko, Zoya N, Gudkov, Andrei V, Blagosklonny, Mikhail V

“…Depending on cellular context, p53-inducing agents (such as nutlin-3a) cause different outcomes including reversible quiescence and irreversible senescence…”
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RNA-binding motif protein 35A is a novel tumor suppressor for colorectal cancer by Leontieva, Olga V., Ionov, Yurij

“…The frequent occurrence of inactivating gene mutations in tumors suggests a tumor suppressor function of the mutated gene.  The RNA binding motif protein 35A…”
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The reconstruction of evolutionary dynamics of processed pseudogenes indicates deep silencing of "retrobiome" in naked mole rat by Kogan, Valeria, Molodtsov, Ivan, Fleyshman, Daria I, Leontieva, Olga V, Koman, Igor E, Gudkov, Andrei V

“…Approximately half of mammalian genomes are occupied by retrotransposons, highly repetitive interspersed genetic elements expanded through the mechanism of…”
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Gerosuppression by pan-mTOR inhibitors by Leontieva, Olga V, Blagosklonny, Mikhail V

“…Rapamycin slows organismal aging and delays age-related diseases, extending lifespan in numerous species. In cells, rapamycin and other rapalogs such as…”
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Weekly administration of rapamycin improves survival and biomarkers in obese male mice on high‐fat diet by Leontieva, Olga V., Paszkiewicz, Geraldine M., Blagosklonny, Mikhail V.

“…Summary Recent discoveries have revealed the key role of mTOR (target of rapamycin) in aging. Furthermore, rapamycin extends lifespan in mice, especially in…”
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DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence by Leontieva, Olga V, Blagosklonny, Mikhail V

“…When the cell cycle is arrested, growth-promoting pathways such as mTOR (Target of Rapamycin) drive cellular senescence, characterized by cellular…”
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Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells by Leontieva, Olga V., Lenzo, Felicia, Demidenko, Zoya N., Blagosklonny, Mikhail V.

“…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…”
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Involvement of the ERK Signaling Cascade in Protein Kinase C-mediated Cell Cycle Arrest in Intestinal Epithelial Cells by Clark, Jennifer A., Black, Adrian R., Leontieva, Olga V., Frey, Mark R., Pysz, Marybeth A., Kunneva, Laura, Woloszynska-Read, Anna, Roy, Durga, Black, Jennifer D.

“…We have reported previously that protein kinase C (PKC) signaling can mediate a program of cell cycle withdrawal in IEC-18 nontransformed intestinal crypt…”
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Yeast-like chronological senescence in mammalian cells: phenomenon, mechanism and pharmacological suppression by Leontieva, Olga V, Blagosklonny, Mikhail V

“…In yeast, chronological senescence (CS) is defined as loss of viability in stationary culture. Although its relevance to the organismal aging remained unclear,…”
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Dual mTORC1/C2 inhibitors suppress cellular geroconversion (a senescence program) by Leontieva, Olga V, Demidenko, Zoya N, Blagosklonny, Mikhail V

“…In proliferating cells, mTOR is active and promotes cell growth. When the cell cycle is arrested, then mTOR converts reversible arrest to senescence…”
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Tumor promoter-induced cellular senescence: cell cycle arrest followed by geroconversion by Leontieva, Olga V, Blagosklonny, Mikhail V

“…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…”
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