Defect in ERK2 and p54JNK activation in aging mouse splenocytes
Author
dc.contributor.author
Li, Min
Author
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Torres, Claudio
Author
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Acuña Castillo, Claudio
Author
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Walter, Robin Ann
Author
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Gardner, Elizabeth M.
Author
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Murasko, Donna M.
Author
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Sierra, Felipe
Admission date
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2019-01-29T17:51:03Z
Available date
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2019-01-29T17:51:03Z
Publication date
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2002
Cita de ítem
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Journals of Gerontology - Series A Biological Sciences and Medical Sciences, Volumen 57, Issue 2, 2018, Pages B41-B47
Identifier
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10795006
Identifier
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10.1093/gerona/57.2.B41
Identifier
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https://repositorio.uchile.cl/handle/2250/163490
Abstract
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We have previously reported on a defect in both extracellular signal-regulated protein kinase (ERK) and c-jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) activation in splenocytes obtained from old rats. In order to investigate whether these effects are conserved across species, we have now used mouse splenocytes to measure the effect of aging on the activation of the same two MAPK families: ERK and JNK. Our results demonstrate that, as in rats, both MAPK signal transduction pathways are affected by aging in mice, indicating the existence of a further defect located downstream of the receptor- proximal events. Whereas ERK1 and p46JNK activation were not significantly modified, the kinetics of both ERK2 and p54JNK activation and inactivation were affected in splenocytes from old animals. Specifically, by analyzing the kinetics of activation and inactivation of these enzymes, we found a nearly 50% decrease in the fold of activation of both ERK2 and p54JNK. These defec