Anti-PINK1 Antibody
$378.00
| Host | Quantity | Applications | Species Reactivity | Data Sheet | |
|---|---|---|---|---|---|
| Rabbit | 100ug | WB | Human |  |
Overview
Product Name Anti-PINK1 Antibody (28116)
Description Anti-PINK1 (PTEN-induced kinase) Rabbit Polyclonal Antibody
Target PINK1
Species Reactivity Human
Applications WB
Host Rabbit
Clonality Polyclonal
Immunogen Synthetic peptide corresponding to amino acids 258-274 (YRKSKRGPKQLAPHPNI) of human PINK1 conjugated to KLH.
Properties
Form Liquid
Concentration Lot Specific
Formulation PBS, pH 7.4.
Buffer Formulation Phosphate Buffered Saline
Buffer pH pH 7.4
Format Purified
Purification Purified by Protein A affinity chromatography
Specificity Information
Specificity This antibody recognizes human PINK1.
Target Name Serine/threonine-protein kinase PINK1, mitochondrial
Target ID PINK1
Uniprot ID Q9BXM7
Alternative Names EC 2.7.11.1, BRPK, PTEN-induced putative kinase protein 1
Gene Name PINK1
Sequence Location Mitochondrion outer membrane, Mitochondrion inner membrane, Cytoplasm, cytosol
Biological Function Serine/threonine-protein kinase which protects against mitochondrial dysfunction during cellular stress by phosphorylating mitochondrial proteins such as PRKN and DNM1L, to coordinate mitochondrial quality control mechanisms that remove and replace dysfunctional mitochondrial components (PubMed:14607334, PubMed:18957282, PubMed:18443288, PubMed:15087508, PubMed:19229105, PubMed:19966284, PubMed:20404107, PubMed:22396657, PubMed:20798600, PubMed:23620051, PubMed:23754282, PubMed:23933751, PubMed:24660806, PubMed:24898855, PubMed:24751536, PubMed:24784582, PubMed:24896179, PubMed:25527291, PubMed:32484300, PubMed:20547144). Depending on the severity of mitochondrial damage and/or dysfunction, activity ranges from preventing apoptosis and stimulating mitochondrial biogenesis to regulating mitochondrial dynamics and eliminating severely damaged mitochondria via mitophagy (PubMed:18443288, PubMed:23620051, PubMed:24898855, PubMed:20798600, PubMed:20404107, PubMed:19966284, PubMed:32484300, PubMed:22396657, PubMed:32047033, PubMed:15087508). Mediates the translocation and activation of PRKN at the outer membrane (OMM) of dysfunctional/depolarized mitochondria (PubMed:19966284, PubMed:20404107, PubMed:20798600, PubMed:23754282, PubMed:24660806, PubMed:24751536, PubMed:24784582, PubMed:25474007, PubMed:25527291). At the OMM of damaged mitochondria, phosphorylates pre-existing polyubiquitin chains at 'Ser-65', the PINK1-phosphorylated polyubiquitin then recruits PRKN from the cytosol to the OMM where PRKN is fully activated by phosphorylation at 'Ser-65' by PINK1 (PubMed:19966284, PubMed:20404107, PubMed:20798600, PubMed:23754282, PubMed:24660806, PubMed:24751536, PubMed:24784582, PubMed:25474007, PubMed:25527291). In damaged mitochondria, mediates the decision between mitophagy or preventing apoptosis by promoting PRKN-dependent poly- or monoubiquitination of VDAC1; polyubiquitination of VDAC1 by PRKN promotes mitophagy, while monoubiquitination of VDAC1 by PRKN decreases mitochondrial calcium influx which ultimately inhibits apoptosis (PubMed:32047033). When cellular stress results in irreversible mitochondrial damage, functions with PRKN to promote clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:14607334, PubMed:20798600, PubMed:20404107, PubMed:19966284, PubMed:23933751, PubMed:15087508). The PINK1-PRKN pathway also promotes fission of damaged mitochondria by phosphorylating and thus promoting the PRKN-dependent degradation of mitochondrial proteins involved in fission such as MFN2 (PubMed:18443288, PubMed:23620051, PubMed:24898855). This prevents the refusion of unhealthy mitochondria with the mitochondrial network or initiates mitochondrial fragmentation facilitating their later engulfment by autophagosomes (PubMed:18443288, PubMed:23620051). Also promotes mitochondrial fission independently of PRKN and ATG7-mediated mitophagy, via the phosphorylation and activation of DNM1L (PubMed:18443288, PubMed:32484300). Regulates motility of damaged mitochondria by promoting the ubiquitination and subsequent degradation of MIRO1 and MIRO2; in motor neurons, this likely inhibits mitochondrial intracellular anterograde transport along the axons which probably increases the chance of the mitochondria undergoing mitophagy in the soma (PubMed:22396657). Required for ubiquinone reduction by mitochondrial complex I by mediating phosphorylation of complex I subunit NDUFA10 (By similarity). {UniProtKB:Q99MQ3, PubMed:14607334, PubMed:15087508, PubMed:18443288, PubMed:18957282, PubMed:19229105, PubMed:19966284, PubMed:20404107, PubMed:20547144, PubMed:20798600, PubMed:22396657, PubMed:23620051, PubMed:23754282, PubMed:23933751, PubMed:24660806, PubMed:24751536, PubMed:24784582, PubMed:24896179, PubMed:24898855, PubMed:25474007, PubMed:25527291, PubMed:32047033, PubMed:32484300}.
Research Areas Neuroscience
Background Mutations in the PTEN-induced kinase (PINK1) gene, which is located within the PARK6 locus on chromosome 1p35- p36, have recently been identified in patients with recessive early onset Parkinson's disease. Data suggest that PINK1 may be the second most common causative gene next to parkin in parkinsonism with the recessive mode of inheritance.
Handling
Storage Store at 2 - 8ºC. Do not Freeze.
Dilution Instructions Dilute in PBS or medium that is identical to that used in the assay system.
Application Instructions Immunoblotting: use at 1:500 dilution. A band of approximately 62-63 kDa is detected.
Positive control: transfected cell lines.
Positive control: transfected cell lines.
References & Data Sheet
References Beilina, A et al. (2005) Proc Natl Acad Sci USA 102: 5703-08. ; Valente, EM et al. (2004) Science 304: 1158-60. Rogaeva, E et al. (2004) Arch Neurol 61: 1898-1904. ; Hatano, Y et al. (2004) Ann Neurol 56: 424-27.
Data Sheet 
Download PDF Data Sheet
Download PDF Data Sheet