Abstract:
:Long-term amino acid starvation represents a form of metabolic stress which stimulates gene expression. Here we report that depriving HeLa cells for any one of a series of amino acids activates c-Jun N-terminal kinase-1 (JNK-1). In contrast, the other mitogen-activated protein kinases (MAPKs) ERK-1 and, to a lesser extent, p38 activities decreased under such conditions. In methionine- or leucine-deprived cells, JNK-1 activation occurred after 4 or 6 h, respectively, and reached a steady maximum of 5- to 7-fold over control cells afterwards. This activation was dependent on the amino acid concentration and it could be reversed by resupplying the complete medium. Limitation for all amino acids also augmented JNK-1 activity, whereas increased amino acid concentrations had an opposite effect. The free radical scavenging thiol antioxidant N-acetylcysteine (NAC) alleviated partially JNK-1 activation in amino acid-deprived cells. The data indicate that activation of JNK-1 by long-term amino acid deprivation may be mediated in part by oxidative stress.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Aubel C,Dehez S,Chabanon H,Seva C,Ferrara M,Brachet Pdoi
10.1016/s0898-6568(01)00159-0subject
Has Abstractpub_date
2001-06-01 00:00:00pages
417-23issue
6eissn
0898-6568issn
1873-3913pii
S0898-6568(01)00159-0journal_volume
13pub_type
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