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SMC-450D-APC

PINK1 Antibody, Clone N4/15: APC

Cannot supply to this region.

SKU:
SMC-450D-APC
Additional Names:
Parkinson disease (autosomal recessive) 6, EC 2.7.11.1, PARK6, serine/threonine-protein kinase PINK1 mitochondrial, PTEN-induced putative kinase protein 1, protein kinase BRPK, BRPK, FLJ27236, PTEN induced putative kinase 1, Phosphatase and Tensin Homolog
Application:
IHC, WB, IF, ICC
Concentration:
1 mg/ml
Species Reactivity:
Human
Purification:
Protein G Purified
Storage Conditions:
See Manual
Supplier:
StressMarq Biosciences
Host:
Mouse
Reactivities:
Human, Mouse, Rat
ABP:
IMP-GEN-2015-06 < 10% Serum <100ml
Buffer:
95.46mM Phosphate, 2.48mM MES and 2mM EDTA
Immunogen:
Fusion protein amino acids 112-496 (cytoplasmic C-terminus) of human PINK1. 82% identical to rat and 81% identical to mouse. >30% identity with DMPK.
Clone:
N4/15 (Formerly sold as S4-15)
Uniprot:
Q9BXM7.1
Synonyms:
BRPK;PARK6;protein kinase BRPK;PTEN induced putative kinase 1;PTEN-induced putative kinase protein 1;serine/threonine-protein kinase PINK1, mitochondrial
Extra Details:
PINK1 (PTEN-induced putative kinase 1) is a mitochondrial serine/threonine kinase that safeguards mitochondrial integrity and function. It plays a central role in mitophagy-the selective autophagic clearance of damaged mitochondria-by phosphorylating mitochondrial substrates and recruiting the cytosolic E3 ubiquitin ligase Parkin to the outer mitochondrial membrane (OMM). PINK1 is synthesized as a 63 kDa precursor and undergoes proteolytic processing to generate cleaved forms that localize to various sub-mitochondrial compartments. Its kinase domain faces the cytosol, enabling interactions with cytosolic proteins involved in mitochondrial quality control. Mutations in PINK1 are linked to autosomal recessive early-onset Parkinson's disease and are associated with mitochondrial dysfunction, alpha-synuclein aggregation, and impaired proteasome activity. Loss of PINK1 function disrupts mitochondrial dynamics and neuronal survival, making it a key target in neurodegenerative disease research.
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