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Creative Biolabs

PINK1 Antibodies

The main pathological changes in Parkinson's disease (PD) are the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, as well as a decrease in dopamine levels in the striatum. Prior research has indicated that the pathophysiology of PD could be caused by mitochondrial malfunction. Under physiological and pathological conditions, the body normally removes dysfunctional mitochondria, reduces oxidative stress levels, and prevents cell death through mitochondrial autophagy. Recent studies have shown that regulation of mitochondrial autophagy can affect neuronal cell apoptosis in Parkinson's patients.

The PINK1 gene (encoding the PINK1 protein) is a known pathogenic variant gene that causes PD. A large number of in vitro and biochemical experiments have shown that PINK1 protects neuronal cells by inducing autophagy of damaged mitochondria, and loss of PINK1 function leads to neuronal cell death in PD.

PINK1 in PD

The 581 amino acid polypeptide known as PINK1 has a hydrophobic transmembrane region that functions as a mitochondrial inner membrane transfer termination signal after an N-terminal that resembles a mitochondrial targeting signal. A serine/threonine domain is made up of residues 156-509, and it is succeeded by a C-terminal domain that functions as a signal for mitochondrial outer membrane retention. The mitochondrial inner membrane protease PARL (presenilin-associated rhomboid-like protein) cleaves PINK1 when it is constantly transported to the inner membrane of normal mitochondria, producing an N-terminal degradation motif that is then removed.

Fig 1 Domain architecture of PINK1 (581 amino acids), Mitochondrial targeting sequence (MTS), transmembrane domain (TMD). (Vizziello, et al., 2021)Fig.1 Domain structure of PINK11,2.

Mutations in PINK1 alter its kinase activity, self-phosphor ubiquitination, substrate binding efficiency, and ability to maintain protein stability, leading to mitochondrial malfunction, including mitochondrial autophagy. Damaged mitochondria continue to accumulate, triggering dopaminergic neuron loss and, ultimately, PD. As a result, maintaining normal levels of mitochondrial autophagy may become an important strategy for treating PD.

PINK1 Antibodies Selection Guide

At Creative Biolabs, you can choose from a wide range of PINK1 antibodies for different applications. Each PINK1 antibody has undergone rigorous multiple validation and quality assurance services. Please browse and select from our catalog of PINK1 monoclonal antibodies. If you cannot find the right product for your research, please contact us now. Our scientists are always ready to customize the most suitable product for you.

Cat. No Product Name Host Application
NAB2007FY533 Mouse Anti-PINK1 Monoclonal Antibody (CBP1966) Mouse WB; IHC; ICC; IF
NAB2010248LS Mouse Anti-Human PINK1 Monoclonal Antibody (CBP2303) Mouse WB; ICC
NAB-0720-Z5467 Rabbit Anti-PINK1 Monoclonal Antibody (CBP3062) Rabbit WB; ICC; IF; IP
NRZP-0922-ZP3758 Anti-PINK1 Antibody, Clone N34042 (CBP15069) Rabbit WB; IP
NRZP-0822-ZP554 Anti-PINK1 Antibody, Clone N30429P (CBP9108) Mouse WB; ICC; IF; IHC; IHC-P; PAGE

See all PINK1 antibodies

References

  1. Vizziello, Maria, et al. "Disruption of mitochondrial homeostasis: The role of PINK1 in Parkinson's disease." Cells 10.11 (2021): 3022.
  2. Image retrieved from Figure 1 "Domain architecture of PINK1 (581 amino acids). Mitochondrial targeting sequence (MTS, orange), transmembrane domain (TMD, blue)." Vizziello et al., 2021, used under [CC BY 4.0](https://creativecommons.org/licenses/by/4.0). The title was changed to "Domain structure of PINK1."
For Research Use Only. Not For Clinical Use.

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