期刊
FEBS LETTERS
卷 590, 期 10, 页码 1455-1466出版社
WILEY
DOI: 10.1002/1873-3468.12177
关键词
Glutathione S-Transferase pi; Nrf2-Keap1 pathway; S-glutathionylation
资金
- Fundacao para a Ciencia e a Tecnologia (FCT), Portugal [PTDC/NEU-OSD/0502/2012]
- iMed.ULisboa from FCT [UID/DTP/04138/2013]
- FCT [SFRH/BPD/98023/2013]
- Fundação para a Ciência e a Tecnologia [PTDC/NEU-OSD/0502/2012, SFRH/BPD/98023/2013] Funding Source: FCT
Oxidative stress is a key pathological feature of Parkinson's disease (PD). Glutathione S-transferase pi (GSTP) is a neuroprotective antioxidant enzyme regulated at the transcriptional level by the antioxidant master regulator nuclear factor-erythroid 2-related factor 2 (Nrf2). Here, we show for the first time that upon MPTP-induced oxidative stress, GSTP potentiates S-glutathionylation of Kelch-like ECH-associated protein 1 (Keap1), an endogenous repressor of Nrf2, in vivo. S-glutathionylation of Keap1 leads to Nrf2 activation and subsequently increases expression of GSTP. This positive feedback regulatory loop represents a novel mechanism by which GSTP elicits antioxidant protection in the brain.
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