Parkin - Role in Mitochondrial Quality Control and Parkinson's Disease

Fri, 11/06/2015 - 14:44

Parkin/PARK2 is a cytosolic enzyme which gets recruited to cellular mitochondria damaged through depolarization, ROS or unfolded proteins accumulation, and exert protective effects by inducing mitophagy (mitochondrial autophagy). Parkin induces mitophagy by promoting mitofission (mitochondrial division) and by ubiquitinating mitochondrial proteins to facilitate their recognition/recruitment to the autophagosomal surface. It is a RING-in-between-RING (RBR) E3 ligase which is capable of mediating mono, multi-mono and polyubiquitylation of several proteins including MFN1, MFN2, Miro, BCL2, SYT11, CCNE1, GPR37, RHOT1/MIRO1, STUB1, SNCAIP, SEPT5, TOMM20, USP30, ZNF746, AIMP2 etc. Mutations in PARK2 gene are the most common cause of autosomal recessive Parkinson’s disease (1). Studies implicating PINK1−/− and Parkin−/− mutant Drosophila flies have shown similar mitochondrial abnormalities, as well as neuronal loss and motor deficits, and that Parkin can complement PINK1 (2).

parkin antibody

Parkin Antibody (1H4) [H00005071-M01]
Western Blot analysis of Parkin/PARK2 protein expression in the whole cell lysate of Jurkat cells (L017V1) using monoclonal Parkin antibody, clone 1H4.

Chen et al 2013 used Parkin antibody for IHC-P and WB assays in experiments involving light-induced retinal degeneration in Abca4−/−Rdh8−/− mice. IHC of retina from albino WT mice demonstrated that Parkin was ubiquitously expressed in the tissue. WB assay for Parkin was employed on retina lysates from Abca4−/−Rdh8−/− mice that were exposed to white light at 10,000 lux for 30 minutes, and when compared to no light group,  up-regulated Parkin expression was observed in response to light exposure (3). Parkin primary transcript has been shown to undergo an extensive alternative splicing, which increases the transcriptomic diversification without gene duplication. Scuderi and coworkers used several Parkin Antibodies as well as published reports for analysis of parkin isoforms expression/distribution in human, rat, and mouse. They further highlighted the biological relevance of Parkin isoforms expression patterns in brain to the differential pathogenetic effects of PARK2 gene mutations (4).

Novus Biologicals offers Parkin reagents for your research needs including:


  1. Martin et al 2011. Recent advances in the genetics of Parkinson's disease. Annu Rev Genomics Hum Genet. 12:301-25
  2. Park et al. 2006. Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin. Nature. 441:1157-1161
  3. Chen et al. 2013. Autophagy protects the retina from light-induced degeneration. J Biol Chem.  288: 7506-18
  4. Scuderi et al. 2014. Alternative splicing generates different parkin protein isoforms: evidences in human, rat, and mouse brain. Biomed Res Int. 2014:690796

By: Subhash Gangar

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