PINK1/Parkin

PTEN-induced kinase 1/Parkin

PINK1 (PTEN-induced kinase 1) is a serine/threonine protein kinase whose activity is affected by mitochondrial membrane potential. PINK1 accumulates on the outer damaged mitochondrial membrane and activates PARKIN through phosphorylation. PARKIN is an E3 ubiquitin ligase that ubiquitinates mitochondrial outer membrane proteins, recruits autophagy-related proteins such as OPTN, NDP52, and initiates mitophagy. PINK1/Parkin regulates mitochondrial homeostasis, selectively removes damaged or redundant mitochondria, thereby maintaining and optimizing the mitochondrial network, regulating the energy metabolism, reducing oxidative stress and inflammatory responses. PINK1/Parkin dysfunction could lead to Parkinson's disease (PD), Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), or glaucoma^[1]^[2].

References:

[1]. Pickrell AM, et al., The roles of PINK1, parkin, and mitochondrial fidelity in Parkinson's disease. Neuron. 2015 Jan 21;85(2):257-73. [Content Brief]

[2]. Quinn PMJ, et al., PINK1/PARKIN signalling in neurodegeneration and neuroinflammation. Acta Neuropathol Commun. 2020 Nov 9;8(1):189. [Content Brief]

PINK1/Parkin Related Products (41):

By Effects:	Inhibitors (5) Activators (23) Modulator (1)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-17355BS

Dexpramipexole-d₃ dihydrochloride	Activator
Dexpramipexole-d₃ ((R)-Pramipexole-d₃) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Na_v1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

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