| Host: |
Rabbit |
| Applications: |
ELISA/IHC/IP/WB |
| Reactivity: |
Human/Mouse |
| Note: |
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
| Short Description: |
Rabbit polyclonal antibody anti-PINK1 is suitable for use in ELISA, Immunohistochemistry, Immunoprecipitation and Western Blot research applications. |
| Clonality: |
Polyclonal |
| Conjugation: |
FITC |
| Isotype: |
IgG |
| Formulation: |
Contains Tris, HCl/Glycine buffer pH 7.4-7.8, 30% Glycerol and 0.5% BSA, along with cryo-protective agents, Hepes, and long-term preservatives (0.02% Sodium Azide). |
| Purification: |
Affinity Purified |
| Concentration: |
0.55-0.75 µg/µl |
| Dilution Range: |
WB: 1:500DB: 1:10, 000ELISA: 1:10, 000IP: 1:200IHC: 1:50-1:150 |
| Storage Instruction: |
Store at-20°C for long term storage. Avoid freeze-thaw cycles. |
| Gene Symbol: |
PINK1 |
| Gene ID: |
65018 |
| Uniprot ID: |
PINK1_HUMAN |
| Immunogen: |
Synthetic peptide corresponding to unique amino acid sequence on human PINK1 protein. |
| Tissue Specificity | Highly expressed in heart, skeletal muscle and testis, and at lower levels in brain, placenta, liver, kidney, pancreas, prostate, ovary and small intestine. Present in the embryonic testis from an early stage of development. |
| Post Translational Modifications | Proteolytically cleaved. In healthy cells, the precursor is continuously imported into the inner mitochondrial membrane (IMM), where it is proteolytically cleaved by mitochondrial-processing peptidase (MPP) and then undergoes further proteolytic cleavage by PARL or AFG3L2 to give rise to the 52 kDa short form. The 52 kDa short form is then released into the cytosol where it rapidly undergoes proteasome-dependent degradation. In unhealthy cells, when cellular stress conditions lead to the loss of mitochondrial membrane potential, mitochondrial import is impaired leading to the precursor accumulating on the outer mitochondrial membrane (OMM). If accumulation at the OMM fails and it is imported into the depolarized mitochondria, it undergoes cleavage by the IMM protease OMA1, promoting its subsequent degradation by the proteasome. Autophosphorylated. Loss of mitochondrial membrane potential results in the precursor accumulating on the outer mitochondrial membrane (OMM) where it is activated by autophosphorylation. Autophosphorylation at Ser-228 and Ser-402 is sufficient and essential for selective recruitment of PRKN to depolarized mitochondria, via PINK1-dependent phosphorylation of ubiquitin and maybe PRKN. |
| Function | Serine/threonine-protein kinase which acts as a sensor of mitochondrial damage and protects against mitochondrial dysfunction during cellular stress. It phosphorylates mitochondrial proteins to coordinate mitochondrial quality control mechanisms that remove and replace dysfunctional mitochondrial components. Depending on the severity of mitochondrial damage, activity ranges from preventing apoptosis and stimulating mitochondrial biogenesis to eliminating severely damaged mitochondria via PINK1-PRKN-dependent mitophagy. When cellular stress results in irreversible mitochondrial damage, PINK1 accumulates at the outer mitochondrial membrane (OMM) where it phosphorylates pre-existing polyubiquitin chains at 'Ser-65', recruits PRKN from the cytosol to the OMM and activates PRKN by phosphorylation at 'Ser-65'.activated PRKN then ubiquinates VDAC1 and other OMM proteins to initiate mitophagy. The PINK1-PRKN pathway also promotes fission of damaged mitochondria through phosphorylation and PRKN-dependent degradation of mitochondrial proteins involved in fission such as MFN2. This prevents the refusion of unhealthy mitochondria with the mitochondrial network or initiates mitochondrial fragmentation facilitating their later engulfment by autophagosomes. Also promotes mitochondrial fission independently of PRKN and ATG7-mediated mitophagy, via the phosphorylation and activation of DNM1L. 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. Required for ubiquinone reduction by mitochondrial complex I by mediating phosphorylation of complex I subunit NDUFA10. Phosphorylates LETM1, positively regulating its mitochondrial calcium transport activity. |
| Protein Name | Serine/Threonine-Protein Kinase Pink1 - MitochondrialBrpkPten-Induced Putative Kinase Protein 1 |
| Database Links | Reactome: R-HSA-5205685Reactome: R-HSA-9614657 |
| Cellular Localisation | Mitochondrion Outer MembraneSingle-Pass Membrane ProteinMitochondrion Inner MembraneCytoplasmCytosolLocalizes Mostly In Mitochondrion And The Two Smaller Proteolytic Processed Fragments Localize Mainly In CytosolUpon Mitochondrial Membrane Depolarization Following DamagePink1 Import Into The Mitochondria Is ArrestedWhich Induces Its Accumulation In The Outer Mitochondrial MembraneWhere It Acquires Kinase Activity |
| Alternative Antibody Names | Anti-Serine/Threonine-Protein Kinase Pink1 - Mitochondrial antibodyAnti-Brpk antibodyAnti-Pten-Induced Putative Kinase Protein 1 antibodyAnti-PINK1 antibody |
Information sourced from Uniprot.org
12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance
