NP_001005560.1
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
83,562 Da
NCBI Official Full Name
85/88 kDa calcium-independent phospholipase A2 isoform 1
NCBI Official Synonym Full Names
phospholipase A2 group VI
NCBI Protein Information
85/88 kDa calcium-independent phospholipase A2
UniProt Protein Name
85/88 kDa calcium-independent phospholipase A2
UniProt Synonym Protein Names
Group VI phospholipase A2; GVI PLA2; Intracellular membrane-associated calcium-independent phospholipase A2 beta; iPLA2-beta; Patatin-like phospholipase domain-containing protein 9; PNPLA9
UniProt Synonym Gene Names
UniProt Entry Name
PLPL9_RAT
NCBI Summary for Pla2g6
has Ca2+ independent phospholipase A2 activity; may play a role in regulating transmembrane ionic fluxes in pancreatic beta cells [RGD, Feb 2006]
UniProt Comments for Pla2g6
PLA2G6: 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. Has a role in cardiolipin (CL) deacylation. Required for both speed and directionality of monocyte MCP1/CCL2-induced chemotaxis through regulation of F- actin polymerization at the pseudopods. Defects in PLA2G6 are the cause of neurodegeneration with brain iron accumulation type 2B (NBIA2B). A neurodegenerative disorder associated with iron accumulation in the brain, primarily in the basal ganglia. It is characterized by progressive extrapyramidal dysfunction leading to rigidity, dystonia, dysarthria and sensorimotor impairment. Defects in PLA2G6 are the cause of neurodegeneration with brain iron accumulation type 2A (NBIA2A); also known as Seitelberger disease. NBIA2A 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. Defects in PLA2G6 are the cause of Parkinson disease type 14 (PARK14). An adult-onset progressive neurodegenerative disorder characterized by parkinsonism, dystonia, severe cognitive decline, cerebral and cerebellar atrophy and absent iron in the basal ganglia on magnetic resonance imaging. 4 isoforms of the human protein are produced by alternative splicing.
Protein type: Lipid Metabolism - alpha-linolenic acid; Lipid Metabolism - ether lipid; EC 3.1.1.4; Phospholipase; Lipid Metabolism - arachidonic acid; Lipid Metabolism - linoleic acid; Lipid Metabolism - glycerophospholipid
Cellular Component: cytoplasm; cytosol; extracellular space; microtubule organizing center; mitochondrial inner membrane; mitochondrion
Molecular Function: ATP-dependent protein binding; calcium-independent phospholipase A2 activity; calmodulin binding; protein kinase binding
Biological Process: antibacterial humoral response; cardiolipin biosynthetic process; chemotaxis; elevation of cytosolic calcium ion concentration; lipid catabolic process; maternal process involved in pregnancy; memory; negative regulation of synaptic transmission, glutamatergic; positive regulation of exocytosis; positive regulation of protein amino acid phosphorylation; positive regulation of vasodilation; urinary bladder smooth muscle contraction
Research Articles on Pla2g6
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Products associated with Pla2g6 elisa kit
Pathways associated with Pla2g6 elisa kit
Diseases associated with Pla2g6 elisa kit
Organs/Tissues associated with Pla2g6 elisa kit
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