Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 286, Issue 40, Pages 35308-35317Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M110.207134
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Funding
- National Natural Sciences Foundation of China [30970921]
- National High-tech Research and Development program of China [2011CB5004102]
- Chinese Academy of Sciences [KSCX2-YW-R138]
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Parkinson disease (PD)- and cancer-associated protein, DJ-1, mediates cellular protection via many signaling pathways. Deletions or mutations in the DJ-1 gene are directly linked to autosomal recessive early-onset PD. DJ-1 has potential roles in mitochondria. Here, we show that DJ-1 increases its mitochondrial distribution in response to ultraviolet B (UVB) irradiation and binds to Bcl-X-L. The interactions between DJ-1 and Bcl-X-L are oxidation-dependent. DJ-1(C106A), a mutant form of DJ-1 that is unable to be oxidized, binds Bcl-X-L much less than DJ-1 does. Moreover, DJ-1 stabilizes Bcl-X-L protein level by inhibiting its ubiquitination and degradation through ubiquitin proteasome system (UPS) in response to UVB irradiation. Furthermore, under UVB irradiation, knockdown of DJ-1 leads to increases of Bcl-X-L ubiquitination and degradation upon UVB irradiation, thereby increasing mitochondrial Bax, caspase-3 activation and PARP cleavage. These data suggest that DJ-1 protects cells against UVB-induced cell death dependent on its oxidation and its association with mitochondrial Bcl-X-L.
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