Rabbit anti Human PINK1 (N-Terminal)

Protects against mitochondrial dysfunction during cellular stress, potentially by phosphorylating mitochondrial proteins. Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy). It is necessary for PARK2 recruitment to dysfunctional mitochondria to initiate their degradation. Defects in PINK1 are the cause of Parkinson disease type 6 (PARK6). A neurodegenerative disorder characterized by parkinsonian signs such as rigidity, resting tremor and bradykinesia. A subset of patients manifest additional symptoms including hyperreflexia, autonomic instability, dementia and psychiatric disturbances. Symptoms show diurnal fluctuation and can improve after sleep.

This product is intended FOR RESEARCH USE ONLY, and FOR TESTS IN VITRO, not for use in diagnostic or therapeutic procedures involving Humans or animals.

1. Matsuda, N., et al. ‘PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy.’ J. Cell. Biol., 189, 211-221 (2010) 2. Vives-Bauza, C., et al. ‘PINK1-dependent recruitment of Parkin to mitochondria in mitophagy.’ Proc. Natl. Acad. Sci. USA, 107, 378-383 (2010) 3. Valente, E.M., et al. ‘PINK1 mutations are associated with sporadic early-onset parkinsonism.’ Ann. Neurol., 56, 336-341 (2004) 4. Song, S., et al. ‘Characterization of PINK1 (PTEN-induced Putative Kinase 1) Mutations Associated with Parkinson Disease in Mammalian Cells and Drosophila.’ J Biol Chem. 288(8): 5660-5672, (2013)