Synthesized peptide derived from the Internal region of human Group VI iPLA2.

Group VI iPLA2 Polyclonal Antibody detects endogenous levels of Group VI iPLA2 protein.

PLA2G6

85/88 kDa calcium-independent phospholipase A2

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

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],

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 compatible with iron deposition in the putamen and substantia nigra.,Function:Catalyzes the release of fatty acids from phospholipids. It has been implicated in normal phospholipid remodeling, nitric oxide-induced or vasopressin-induced arachidonic acid release and in leukotriene and prostaglandin production. May participate in fas mediated apoptosis and in regulating transmembrane ion flux in glucose-stimulated B-cells.,Function:Isoform ankyrin-iPLA2-1 and isoform ankyrin-iPLA2-2, which lack the catalytic domain, are probably involved in the negative regulation of iPLA2 activity.,similarity:Contains 7 ANK repeats.,subunit:Forms large oligomeric 270-350 kDa structures.,tissue specificity:Four different transcripts were found to be expressed in a distinct tissue distribution.,

Cytoplasm . Cell membrane . Mitochondrion . Cell projection, pseudopodium . Recruited to the membrane-enriched pseudopods upon MCP1/CCL2 stimulation in monocytes. .

>>Glycerophospholipid metabolism ;
>>Ether lipid metabolism ;
>>Arachidonic acid metabolism ;
>>Linoleic acid metabolism ;
>>alpha-Linolenic acid metabolism ;
>>Metabolic pathways ;
>>Ras signaling pathway ;
>>Vascular smooth muscle contraction ;
>>Fc gamma R-mediated phagocytosis ;
>>Inflammatory mediator regulation of TRP channels