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Torii S, Kasai S, Suzuki A, et al. Involvement of inhibitory PAS domain protein in neuronal cell death in Parkinson's disease. Cell Death Discov. 2015;1:15015doi: 10.1038/cddiscovery.2015.15.
Torii, S., Kasai, S., Suzuki, A., Todoroki, Y., Yokozawa, K., Yasumoto, K. I., Seike, N., Kiyonari, H., Mukumoto, Y., Kakita, A., & Sogawa, K. (2015). Involvement of inhibitory PAS domain protein in neuronal cell death in Parkinson's disease. Cell death discovery, 115015. https://doi.org/10.1038/cddiscovery.2015.15
Torii, S, et al. "Involvement of inhibitory PAS domain protein in neuronal cell death in Parkinson's disease." Cell death discovery vol. 1 (2015): 15015. doi: https://doi.org/10.1038/cddiscovery.2015.15
Torii S, Kasai S, Suzuki A, Todoroki Y, Yokozawa K, Yasumoto KI, Seike N, Kiyonari H, Mukumoto Y, Kakita A, Sogawa K. Involvement of inhibitory PAS domain protein in neuronal cell death in Parkinson's disease. Cell Death Discov. 2015 Aug 17;1:15015. doi: 10.1038/cddiscovery.2015.15. eCollection 2015. PMID: 27551449; PMCID: PMC4981001.
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Cell Death Discov. 2015 Aug 17;1:15015. doi: 10.1038/cddiscovery.2015.15. eCollection 2015.

Involvement of inhibitory PAS domain protein in neuronal cell death in Parkinson's disease.

Cell death discovery

S Torii, S Kasai, A Suzuki, Y Todoroki, K Yokozawa, K-I Yasumoto, N Seike, H Kiyonari, Y Mukumoto, A Kakita, K Sogawa

Affiliations

  1. Department of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University , Sendai, Japan.
  2. Department of Pathology, Brain Research Institute, University of Niigata , Niigata, Japan.
  3. Animal Resource Development Unit, RIKEN Center for Life Science Technologies, Kobe, Japan; Genetic Engineering Team, RIKEN Center for Life Science Technologies, Kobe, Japan.
  4. Genetic Engineering Team, RIKEN Center for Life Science Technologies , Kobe, Japan.

PMID: 27551449 PMCID: PMC4981001 DOI: 10.1038/cddiscovery.2015.15

Abstract

Inhibitory PAS domain protein (IPAS), a repressor of hypoxia-inducible factor-dependent transcription under hypoxia, was found to exert pro-apoptotic activity in oxidative stress-induced cell death. However, physiological and pathological processes associated with this activity are not known. Here we show that IPAS is a key molecule involved in neuronal cell death in Parkinson's disease (PD). IPAS was ubiquitinated by Parkin for proteasomal degradation following carbonyl cyanide m-chlorophenyl hydrazone treatment. Phosphorylation of IPAS at Thr12 by PTEN-induced putative kinase 1 (PINK1) was required for ubiquitination to occur. Activation of the PINK1-Parkin pathway attenuated IPAS-dependent apoptosis. IPAS was markedly induced in the midbrain following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration, and IPAS-deficient mice showed resistance to MPTP-induced degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). A significant increase in IPAS expression was found in SNpc neurons in patients with sporadic PD. These results indicate a mechanism of neurodegeneration in PD.

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