Crosstalk between JNK and SUMO signaling pathways: deSUMOylation is protective against H2O2-induced cell injury.

ABSTRACT:

Background

Oxidative stress is a key feature in the pathogenesis of several neurological disorders. Following oxidative stress stimuli a wide range of pathways are activated and contribute to cellular death. The mechanism that couples c-Jun N-terminal kinase (JNK) signaling, a key pathway in stress conditions, to the small ubiquitin-related modifier (SUMO), an emerging protein in the field, is largely unknown.

Methodology/principal findings

With this study we investigated if SUMOylation participates in the regulation of JNK activation as well as cellular death in a model of H(2)O(2) induced-oxidative stress. Our data show that H(2)O(2) modulates JNK activation and induces cellular death in neuroblastoma SH-SY5Y cells. Inhibition of JNK's action with the D-JNKI1 peptide rescu

SUBMITTER: Feligioni M 

PROVIDER: S-EPMC3229511 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature