Reactive species
Human;Mouse;Rat
Antibody type
Polyclonal Antibody
Protein name
85/88 kDa calcium-independent phospholipase A2
Immunogen
Synthesized peptide derived from the Internal region of human Group VI iPLA2.
Specificity
Group VI iPLA2 Polyclonal Antibody detects endogenous levels of Group VI iPLA2 protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
Western Blot: 1/500 - 1/2000. ELISA: 1/5000. Not yet tested in other applications.
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Other name
PLA2G6; PLPLA9; 85/88 kDa calcium-independent phospholipase A2; CaI-PLA2; Group VI phospholipase A2; GVI PLA2; Intracellular membrane-associated calcium-independent phospholipase A2 beta; iPLA2-beta; Patatin-like phospholipase domain-contai
Background
The protein encoded by this gene is an A2 phospholipase, a class of enzyme that catalyzes the release of fatty acids from phospholipids. The encoded protein may play a role in phospholipid remodelling, arachidonic acid release, leukotriene and prostaglandin synthesis, fas-mediated apoptosis, and transmembrane ion flux in glucose-stimulated B-cells. Several transcript variants encoding multiple isoforms have been described, but the full-length nature of only three of them have been determined to date. [provided by RefSeq, Dec 2010],
Function
catalytic activity:Phosphatidylcholine + H(2)O = 1-acylglycerophosphocholine + a carboxylate.,disease:Defects in PLA2G6 are a cause of neurodegeneration with brain iron accumulation (NBIA) [MIM:610217]. NBIA comprises a clinically and genetically heterogeneous group of disorders with high basal ganglia iron.,disease:Defects in PLA2G6 are the cause of infantile neuroaxonal dystrophy 1 (INAD1) [MIM:256600]; also known as Seitelberger disease. Infantile neuroaxonal dystrophy (INAD) is a neurodegenerative disease characterized by pathologic axonal swelling and spheroid bodies in the central nervous system. Onset is within the first 2 years of life with death by age 10 years.,disease:Defects in PLA2G6 are the cause of Karak syndrome [MIM:608395]. Karak syndrome is a neurologic disease characterized by early-onset progressive cerebellar ataxia, dystonia, spasticity, intellectual and features c
