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Disturbances in mitochondrial potential and changes in calcium signaling are dependent on iPLA2 activity in an animal model of infantile neuroaxonal dystrophy.
The antinociceptive effect of maprotiline was abrogated by iPLA2 antisense oligonucleotide injection to the prefrontal cortex, indicating a role of this enzyme in antinociception. In contrast, injection of iPLA2 antisense oligonucleotide to the somatosensory cortex did not reduce the antinociceptive effect of maprotiline.
The absence of iPLA2beta promotes macrophage M2 polarization.
Time lapse microscopy and integrin endocytosis assay revealed the essential role of calcium-independent phospholipase A2 (show LYPLA1 Proteins) activity for the recycling of alpha 6 integrin-GFP from the endosomal recycling complex to the plasma membrane.
iPLA2-gamma (show PNPLA8 Proteins) has a protective functional role in the normal glomerulus and in glomerulonephritis.
Results suggest that the degeneration of dopaminergic neurons occurs mainly in the distal region of axons in iPLA2beta-KO mice.
This study showed that the absence of iPLA2beta activity does not influence myocardial inflammation, but iPLA2beta is essential for T. cruzi clearance.
Results support the deleterious role of iPLA2beta in severe obesity associated NAFLD.
Genetic or molecular impairment of PLA2g6-dependent Ca(2+) signalling is a trigger for autophagic dysfunction, progressive loss of dopamine (show CA2 Proteins)rgic (DA) neurons in substantia nigra pars compacta and age-dependent L-DOPA-sensitive motor dysfunction.
An inactivation of iPLA2beta exacerbated pathogenesis of experimental colitis by promoting intestinal epithelial cell apoptosis, inhibiting crypt cell regeneration, and causing damage to mucus barrier allowing an activation of innate immune response.
the association of PLA2G6 with the pathogenesis of idiopathic PD, in addition to PARK14.
A novel missense mutation in PLA2G6 gene (c.3G > T:p.M1I) in one and half-year-old boy with muscle weakness and neurodevelopmental regression (speech, motor and cognition).
PLA2G6 mutations in Indian patients with infantile neuroaxonal dystrophy and atypical late-onset neuroaxonal dystrophy
These results strongly suggest that PNPLA9, -6 and -4 play a key role in GPL (show IL31RA Proteins) turnover and homeostasis in human cells. A hypothetical model suggesting how these enzymes could recognize the relative concentration of the different GPLs is proposed
This study identifies a novel PLA2G6 mutation that is the possible genetic cause of FCMTE in this Chinese family.
Finding suggest the broadness of the clinical spectrum of group VI phospholipases A2 (PLA2G6)-related neurodegeneration.
A homozygous novel mutation at position c.2277-1G>C in PLA2G6 gene presumed to give rise to altered splicing, was detected, thus confirming the diagnosis of infantile Neuroaxonal Dystrophy (INAD).
Three catalytically active cPLA2 (show PLA2G4A Proteins), iPLA2, and sPLA2 (show PLA2G2A Proteins) are expressed in different areas within the human spermatozoon cell body. Spermatozoa with a significant low motility showed strong differences both in terms of total specific activity and of different intracellular distribution, compared with normal spermatozoa. Phospholipases could be potential biomarkers of asthenozoospermia.
This study demonstrated that elevated expression of alphaSyn/PalphaSyn in mitochondria appears to be the early response to PLA2G6-deficiency in neurons.
Stimulation of adrenoreceptors causes increased iPLA2 expression via MAP kinase/ERK (show MAPK1 Proteins) 1 (show MAPK3 Proteins)/2.
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.
85 kDa calcium-independent phospholipase A2
, patatin-like phospholipase domain containing 9
, phospholipase A2, group 6 (cytosolic, calcium-independent)
, phospholipase A2, group VI (cytosolic, calcium-independent)
, 85 kDa calcium-independent phospholipase A2-like
, 85/88 kDa calcium-independent phospholipase A2
, GVI PLA2
, group VI phospholipase A2
, intracellular membrane-associated calcium-independent phospholipase A2 beta
, patatin-like phospholipase domain-containing protein 9
, calcium-independent phospholipase A2
, cytosolic, calcium-independent phospholipase A2
, neurodegeneration with brain iron accumulation 2