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921por Shlush, Liran I, Itzkovitz, Shalev, Cohen, Ariel, Rutenberg, Aviad, Berkovitz, Ron, Yehezkel, Shiran, Shahar, Hofit, Selig, Sara, Skorecki, Karl“…Several markers can be used to identify senescent cells, of which the most widely used is the senescence-associated β-galactosidase (SABG) activity. …”
Publicado 2011
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922
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923por Maeda, Yasuhiro, Kawauchi, Masaya, Hirase, Chikara, Yamaguchi, Terufumi, Miyatake, Jun-ichi, Matsumura, ItaruEnlace del recurso
Publicado 2011
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924“…Although the changes observed in senescent cells are likely to result in significant phenotypic alterations, the studies on consequences of endothelial senescence, especially in relation to aging-associated diseases, are scarce. …”
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925por Calvi, Carla L., Podowski, Megan, D'Alessio, Franco R., Metzger, Shana L., Misono, Kaori, Poonyagariyagorn, Hataya, Lopez-Mercado, Armando, Ku, Therese, Lauer, Thomas, Cheadle, Christopher, Talbot, C. Conover, Jie, Chunfa, McGrath-Morrow, Sharon, King, Landon S., Walston, Jeremy, Neptune, Enid R.“…METHODS/PRINCIPAL FINDINGS: Using a murine model of the aging lung, senescent DBA/2 mice, we correlated a longitudinal survey of airspace size and injury measures with a transcriptome from the aging lung at 2, 4, 8, 12, 16 and 20 months of age. …”
Publicado 2011
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926“…Prematurely senescent cells induced by autophagy impairment exhibited the senescent phenotypes, similar to the replicatively senescent cells, such as increased senescence associated β-galactosidase (SA-β-gal) activity, reactive oxygen species (ROS) generation, and accumulation of lipofuscin. …”
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927“…Remarkably, progerin expression and senescence phenotypes are lost in iPSCs but not in differentiated progeny. …”
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928“…Senescence can therefore be thought of in beneficial terms as a tumour suppressor. …”
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929por LLeonart, Matilde E., Carnero, Amancio, Paciucci, Rosanna, Wang, Zhao-Qi, Shomron, NoamEnlace del recurso
Publicado 2011
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930“…BACKGROUND: Cells that reach “Hayflick limit” of proliferation, known as senescent cells, possess a particular type of nuclear architecture. …”
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931“…The role of nuclear factor-κB in cellular senescence is controversial, as it has been associated with both proliferation and tumour progression, and also with growth arrest and ageing. …”
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932por Kaul, Zeenia, Cesare, Anthony J, Huschtscha, Lily I, Neumann, Axel A, Reddel, Roger R“…Replicative senescence is accompanied by a telomere-specific DNA damage response (DDR). …”
Publicado 2012
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933
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934“…Also, certain physiological stimuli, such as transforming growth factor-β, are able to modulate cellular senescence. Currently, the cellular aging process is being widely studied to identify novel molecular markers whose changes correlate with senescence. …”
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935“…In this study, we show that the activity of autophagy increases in H(2)O(2) or RasV12-induced senescent fibroblasts. Inhibiting autophagy promotes cell apoptosis in senescent cells, suggesting that autophagy activation plays a cytoprotective role. …”
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936“…However, studies of senescence have been impeded by the lack of simple, exclusive biomarkers of the senescent state. …”
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937“…Telomere lengths, used as a marker of cellular senescence, were determined using Southern blot analyses. …”
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938“…The molecular mechanism mediating expression of senescent cell antigen-aggregated or cleaved band 3 and externalized phosphatidylserine (PS) on the surface of aged erythrocytes and their premature expression in certain anemias is not completely elucidated. …”
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939por Sheerin, Angela N, Smith, S Kaye, Jennert-Burston, Katrin, Brook, Amy J, Allen, Marcus C, Ibrahim, Badr, Jones, Dawn, Wallis, Corrin, Engelmann, Katrin, Rhys-Williams, William, Faragher, Richard G A, Kipling, David“…Accordingly, a comprehensive investigation of the signalling pathways and mechanisms underpinning proliferative lifespan and senescence in HCEC was undertaken. The effects of exogenous human telomerase reverse transcriptase expression, p53 knockdown, disruption of the pRb pathway by over-expression of CDK4 and reduced oxygen concentration on the lifespan of primary HCEC were evaluated. …”
Publicado 2012
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940por Albertini, Eva, Kozieł, Rafał, Dürr, Angela, Neuhaus, Michael, Jansen-Dürr, Pidder“…Here we show that depletion of cystathionine beta synthase (CBS), a rate limiting enzyme in the reverse transsulfuration pathway, induces premature senescence in human endothelial cells. We found that CBS depletion induces mild mitochondrial dysfunction and increases the sensitivity of endothelial cells to homocysteine, a known inducer of endothelial cell senescence and an established risk factor for vascular disease. …”
Publicado 2012
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