Ignet

Gene Information

Gene symbol: PLA2G4A

Gene name: phospholipase A2, group IVA (cytosolic, calcium-dependent)

HGNC ID: 9035

Synonyms: cPLA2-alpha

Related Genes

#	Gene Symbol	Number of hits
1	ABCA4	1 hits
2	ABCC1	1 hits
3	ADIPOQ	1 hits
4	ARNTL2	1 hits
5	ATP2A3	1 hits
6	CD9	1 hits
7	COX8A	1 hits
8	ENPP2	1 hits
9	GPR55	1 hits
10	IGKV2D-29	1 hits
11	INS	1 hits
12	MAPK1	1 hits
13	MAPK14	1 hits
14	MIA3	1 hits
15	NOS2A	1 hits
16	NOS3	1 hits
17	PIP5K1C	1 hits
18	PLA2G1B	1 hits
19	PPA1	1 hits
20	PPARG	1 hits
21	PRKCA	1 hits
22	PTGS2	1 hits
23	STN	1 hits
24	TFAP2A	1 hits

Related Sentences

#	PMID	Sentence
1	6390059	SZ-induced diabetes also increased acyl-CoA;1-acylglycerol 3-phosphorylcholine acyltransferase (GPCAT) activity (38-45 per cent, p less than 0.01) with 3 different acyl-CoA donors: oleoyl-CoA, linoleoyl-CoA and arachidonoyl-CoA. 1-acyl-GPAT and GPCAT activity returned to normal with insulin treatment.
2	6390059	In contrast to the increased activity of the microsomal fatty acyl-transferases 1-acyl-GPAT and GPCAT, SZ-induced diabetes decreased mitochondrial phospholipase A2 activity and lysophospholipase activity (49-70 per cent, p less than 0.01).
3	6390059	Insulin treatment of the diabetic rats corrected the decreased lysophospholipase and stimulated phospholipase A2 activity 35 per cent higher than controls.
4	6390059	SZ-induced diabetes also increased acyl-CoA;1-acylglycerol 3-phosphorylcholine acyltransferase (GPCAT) activity (38-45 per cent, p less than 0.01) with 3 different acyl-CoA donors: oleoyl-CoA, linoleoyl-CoA and arachidonoyl-CoA. 1-acyl-GPAT and GPCAT activity returned to normal with insulin treatment.
5	6390059	In contrast to the increased activity of the microsomal fatty acyl-transferases 1-acyl-GPAT and GPCAT, SZ-induced diabetes decreased mitochondrial phospholipase A2 activity and lysophospholipase activity (49-70 per cent, p less than 0.01).
6	6390059	Insulin treatment of the diabetic rats corrected the decreased lysophospholipase and stimulated phospholipase A2 activity 35 per cent higher than controls.
7	7635966	Identification of the mechanism for the inhibition of Na+,K(+)-adenosine triphosphatase by hyperglycemia involving activation of protein kinase C and cytosolic phospholipase A2.
8	7635966	The present study tested the hypothesis that the inhibition of Na+,K(+)-ATPase activity is mediated by the sequential activation of PKC and cytosolic phospholipase A2 (cPLA2).
9	7635966	Identification of the mechanism for the inhibition of Na+,K(+)-adenosine triphosphatase by hyperglycemia involving activation of protein kinase C and cytosolic phospholipase A2.
10	7635966	The present study tested the hypothesis that the inhibition of Na+,K(+)-ATPase activity is mediated by the sequential activation of PKC and cytosolic phospholipase A2 (cPLA2).
11	9133554	Herein, we provide the evidence that mitogen-activated protein kinase (MAPK) cascade, an important kinase cascade downstream to PKC and an activator of cytosolic phospholipase A2 (cPLA2) by direct phosphorylation, is activated in glomeruli isolated from streptozotocin-induced diabetic rats.
12	9133554	Furthermore, the activities of cPLA2 also increased in cells cultured under the same conditions and this activation was inhibited by both calphostin C and PD 098059, an inhibitor of MEK (MAPK or extracellular signal-regulated kinase [ERK] kinase).
13	9133554	Activated MAPK, in turn, may induce various functional changes of mesangial cells at least through the activation of cPLA2 and contribute to the development of diabetic nephropathy.
14	9150250	Positional distribution of labelled palmitate from sn-1 position palmitate-labelled lysophosphatidylcholine showed distribution to both sn-1 and sn-2 position of the phosphatidylcholine formed with a significantly increased sn-2 position labelling in diabetes.
15	9150250	In preparations from diabetic animals phosphatidylethanolamine formed in this manner was increased in the presence of an inhibitor of cytosolic phospholipase A2, indicating that it may provide a substrate for phospholipase A2 activity; an effect not seen in cultured cells maintained at raised glucose concentrations.
16	10482042	In view of the potential role of prostaglandins (PGs) in development of glomerular hyperfiltration leading to diabetic nephropathy, we studied the temporal relationship of the activity of cytosolic phospholipase A2 (cPLA2), a rate-limiting enzyme for eicosanoid biosynthesis, with hyperfiltration and the histological changes in glomeruli using OLETF rats, a model for non-insulin-dependent diabetes mellitus (NIDDM).
17	12957654	Activation of p38 mitogen-activated protein kinase/cytosolic phospholipase A2 cascade in hydroperoxide-stressed platelets.
18	12957654	Exogenous 12-HpETE activated platelet p38 mitogen-activated protein kinase (p38 MAPK), as assessed by its phosphorylation, at a concentration as low as 100 nM and was much more potent than hydrogen peroxide.
19	12957654	Moreover, the incubation of platelets with 100 nM 12-HpETE for 2 min led to the phosphorylation of cytosolic phospholipase A2 (cPLA2).
20	12957654	Additionally, decreasing glutathione peroxidase activity pharmacologically favored endogenous 12-HpETE formation and led to an increase in phosphorylated p38 MAPK, while a thiol-reducing agent such as N-acetyl-cysteine fully prevented it.
21	12957654	Finally, significant activation of p38 MAPK was also observed in platelets from type 2 diabetic patients with mild hyperglycemia.
22	12957654	In conclusion, our data provide a new insight into the mechanism of 12-HpETE-induced platelet priming, suggesting that hydroperoxide-induced p38 MAPK activation could play a relevant role in the exacerbated platelet activation associated with oxidative stress as found in diabetes.
23	12957654	Activation of p38 mitogen-activated protein kinase/cytosolic phospholipase A2 cascade in hydroperoxide-stressed platelets.
24	12957654	Exogenous 12-HpETE activated platelet p38 mitogen-activated protein kinase (p38 MAPK), as assessed by its phosphorylation, at a concentration as low as 100 nM and was much more potent than hydrogen peroxide.
25	12957654	Moreover, the incubation of platelets with 100 nM 12-HpETE for 2 min led to the phosphorylation of cytosolic phospholipase A2 (cPLA2).
26	12957654	Additionally, decreasing glutathione peroxidase activity pharmacologically favored endogenous 12-HpETE formation and led to an increase in phosphorylated p38 MAPK, while a thiol-reducing agent such as N-acetyl-cysteine fully prevented it.
27	12957654	Finally, significant activation of p38 MAPK was also observed in platelets from type 2 diabetic patients with mild hyperglycemia.
28	12957654	In conclusion, our data provide a new insight into the mechanism of 12-HpETE-induced platelet priming, suggesting that hydroperoxide-induced p38 MAPK activation could play a relevant role in the exacerbated platelet activation associated with oxidative stress as found in diabetes.
29	15700135	Potential involvement of adipocyte insulin resistance in obesity-associated up-regulation of adipocyte lysophospholipase D/autotaxin expression.
30	16893914	This subinterval contains the circadian rhythm-related transcription factor Arntl2 (Bmal2), a homologue of the type 2 diabetes-associated ARNT (HIF1beta) gene.
31	16893914	Arntl2 upregulation was not associated with changes in the expression levels of other circadian genes in the spleen, but did correlate with the upregulation of the ARNT-binding motif containing Pla2g4a gene, which has recently been described as being protective for the progression of insulitis and autoimmune diabetes in the NOD mouse via regulation of the tumour necrosis factor-alpha pathway.
32	16966336	This effect was mediated by induction of cyclooxygenase-2 (COX-2) gene expression and production of prostaglandin E2 (PGE2) that in turn transactivated epidermal growth factor receptor (EGFR) and Akt.
33	16966336	In support of this, inhibition of COX-2, EGFR, and Akt prevented the PPARdelta-induced cell growth.
34	16966336	Furthermore, PPARdelta activation or PGE2 treatment induced the phosphorylation of cytosolic phospholipase A2alpha (cPLA2alpha), a key enzyme that releases arachidonic acid (AA) substrate for PG production via COX.
35	16966336	Taken together, these observations reveal that PPARdelta induces COX-2 expression in human cholangiocarcinoma cells and that the COX-2-derived PGE2 further activates PPARdelta through phosphorylation of cPLA2alpha.
36	16966336	This effect was mediated by induction of cyclooxygenase-2 (COX-2) gene expression and production of prostaglandin E2 (PGE2) that in turn transactivated epidermal growth factor receptor (EGFR) and Akt.
37	16966336	In support of this, inhibition of COX-2, EGFR, and Akt prevented the PPARdelta-induced cell growth.
38	16966336	Furthermore, PPARdelta activation or PGE2 treatment induced the phosphorylation of cytosolic phospholipase A2alpha (cPLA2alpha), a key enzyme that releases arachidonic acid (AA) substrate for PG production via COX.
39	16966336	Taken together, these observations reveal that PPARdelta induces COX-2 expression in human cholangiocarcinoma cells and that the COX-2-derived PGE2 further activates PPARdelta through phosphorylation of cPLA2alpha.
40	17144165	Extracellular LPA-synthesis is catalyzed by a lysophospholipase D secreted by adipocytes: autotaxin (ATX).
41	17208043	Secretion and lysophospholipase D activity of autotaxin by adipocytes are controlled by N-glycosylation and signal peptidase.
42	17208043	Autotaxin (ATX) is a lysophospholipase D involved in synthesis of lysophosphatidic acid (LPA).
43	17208043	In addition, N-glycosidase treatment and point deletion of the amino-acid N410 inhibits the lysophospholipase D activity of ATX.
44	17208043	Treatment of adipocytes with the furin inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethylketone does not modified secretion or lysophospholipase D activity of ATX.
45	17208043	Transfection in Cos-7 cells of site-directed deleted ATX shows that the furin recognition site is not required for secretion or lysophospholipase D activity of ATX.
46	17208043	Secretion and lysophospholipase D activity of autotaxin by adipocytes are controlled by N-glycosylation and signal peptidase.
47	17208043	Autotaxin (ATX) is a lysophospholipase D involved in synthesis of lysophosphatidic acid (LPA).
48	17208043	In addition, N-glycosidase treatment and point deletion of the amino-acid N410 inhibits the lysophospholipase D activity of ATX.
49	17208043	Treatment of adipocytes with the furin inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethylketone does not modified secretion or lysophospholipase D activity of ATX.
50	17208043	Transfection in Cos-7 cells of site-directed deleted ATX shows that the furin recognition site is not required for secretion or lysophospholipase D activity of ATX.
51	17208043	Secretion and lysophospholipase D activity of autotaxin by adipocytes are controlled by N-glycosylation and signal peptidase.
52	17208043	Autotaxin (ATX) is a lysophospholipase D involved in synthesis of lysophosphatidic acid (LPA).
53	17208043	In addition, N-glycosidase treatment and point deletion of the amino-acid N410 inhibits the lysophospholipase D activity of ATX.
54	17208043	Treatment of adipocytes with the furin inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethylketone does not modified secretion or lysophospholipase D activity of ATX.
55	17208043	Transfection in Cos-7 cells of site-directed deleted ATX shows that the furin recognition site is not required for secretion or lysophospholipase D activity of ATX.
56	17208043	Secretion and lysophospholipase D activity of autotaxin by adipocytes are controlled by N-glycosylation and signal peptidase.
57	17208043	Autotaxin (ATX) is a lysophospholipase D involved in synthesis of lysophosphatidic acid (LPA).
58	17208043	In addition, N-glycosidase treatment and point deletion of the amino-acid N410 inhibits the lysophospholipase D activity of ATX.
59	17208043	Treatment of adipocytes with the furin inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethylketone does not modified secretion or lysophospholipase D activity of ATX.
60	17208043	Transfection in Cos-7 cells of site-directed deleted ATX shows that the furin recognition site is not required for secretion or lysophospholipase D activity of ATX.
61	17208043	Secretion and lysophospholipase D activity of autotaxin by adipocytes are controlled by N-glycosylation and signal peptidase.
62	17208043	Autotaxin (ATX) is a lysophospholipase D involved in synthesis of lysophosphatidic acid (LPA).
63	17208043	In addition, N-glycosidase treatment and point deletion of the amino-acid N410 inhibits the lysophospholipase D activity of ATX.
64	17208043	Treatment of adipocytes with the furin inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethylketone does not modified secretion or lysophospholipase D activity of ATX.
65	17208043	Transfection in Cos-7 cells of site-directed deleted ATX shows that the furin recognition site is not required for secretion or lysophospholipase D activity of ATX.
66	18931027	Pioglitazone protects the myocardium against ischemia-reperfusion injury in eNOS and iNOS knockout mice.
67	18931027	Endothelial nitric oxide synthase (eNOS) activation with subsequent inducible NOS (iNOS), cytosolic phospholipase A2 (cPLA2), and cyclooxygenase-2 (COX2) activation is essential to statin inhibition of myocardial infarct size (IS).
68	18931027	In the rat, the peroxisome proliferator-activated receptor-gamma agonist pioglitazone (Pio) limits IS, upregulates and activates cPLA2 and COX2, and increases myocardial 6-keto-PGF1alpha levels without activating eNOS and iNOS.
69	18931027	Male C57BL/6 wild-type (WT), eNOS-/-, and iNOS-/- mice received 10 mg.kg(-1).day(-1) Pio (Pio+) or water alone (Pio-) for 3 days.
70	18931027	As a result, Pio reduced IS in the WT (15.4+/-1.4% vs. 39.0+/-1.1%; P<0.001), as well as in the eNOS-/- (32.0+/-1.6% vs. 44.2+/-1.9%; P<0.001) and iNOS-/- (18.0+/-1.2% vs. 45.5+/-2.3%; P<0.001) mice.
71	18931027	The protective effect of Pio in eNOS-/- mice was smaller than in the WT (P<0.001) and iNOS-/- (P<0.001) mice.
72	18931027	Pio increased myocardial Ser633 and Ser1177 phosphorylated eNOS levels in the WT and iNOS-/- mice. iNOS was undetectable in all six groups.
73	18931027	Pio increased cPLA2, COX2, and PGI2 synthase levels in the WT, as well as in the eNOS-/- and iNOS-/-, mice.
74	18931027	Pio increased the myocardial 6-keto-PGF1alpha levels and cPLA2 and COX2 activity in the WT, eNOS-/-, and iNOS-/- mice.
75	18931027	In conclusion, the myocardial protective effect of Pio is iNOS independent and may be only partially dependent on eNOS.
76	19560328	To investigate a genetic link between these two diseases, the combined effects of the PLA2G4A, PTGS2 and PPARG genes were tested among 221 British nuclear families consisting of fathers, mothers and affected offspring with schizophrenia.
77	19560328	Eight SNPs detected across the PPARG gene did not show allelic association with schizophrenia; a weak association was detected at rs2745557 in the PTGS2 locus (chi2=4.19, p=0.041) and rs10798059 in the PLA2G4A locus (chi2=4.28, p=0.039) but these associations did not survive after 10,000 permutations to correct the p-value (global p=0.246).
78	19560328	The gene-gene interaction test did not show any evidence of either cis-phase interactions for the PLA2G4A and PTGS2 combinations or a trans-phase interaction for the PLA2G4A and PPARG combinations.
79	19560328	To investigate a genetic link between these two diseases, the combined effects of the PLA2G4A, PTGS2 and PPARG genes were tested among 221 British nuclear families consisting of fathers, mothers and affected offspring with schizophrenia.
80	19560328	Eight SNPs detected across the PPARG gene did not show allelic association with schizophrenia; a weak association was detected at rs2745557 in the PTGS2 locus (chi2=4.19, p=0.041) and rs10798059 in the PLA2G4A locus (chi2=4.28, p=0.039) but these associations did not survive after 10,000 permutations to correct the p-value (global p=0.246).
81	19560328	The gene-gene interaction test did not show any evidence of either cis-phase interactions for the PLA2G4A and PTGS2 combinations or a trans-phase interaction for the PLA2G4A and PPARG combinations.
82	19560328	To investigate a genetic link between these two diseases, the combined effects of the PLA2G4A, PTGS2 and PPARG genes were tested among 221 British nuclear families consisting of fathers, mothers and affected offspring with schizophrenia.
83	19560328	Eight SNPs detected across the PPARG gene did not show allelic association with schizophrenia; a weak association was detected at rs2745557 in the PTGS2 locus (chi2=4.19, p=0.041) and rs10798059 in the PLA2G4A locus (chi2=4.28, p=0.039) but these associations did not survive after 10,000 permutations to correct the p-value (global p=0.246).
84	19560328	The gene-gene interaction test did not show any evidence of either cis-phase interactions for the PLA2G4A and PTGS2 combinations or a trans-phase interaction for the PLA2G4A and PPARG combinations.
85	20005724	Autotaxin (ATX) is a member of the ecto-nucleotide pyrophosphatase/phosphodiesterase (NPP) family and is a lysophospholipase D that cleaves the choline headgroup from lysophosphatidylcholine to generate the bioactive lipid lysophosphatidic acid (LPA).
86	20435073	AGE-BSA (40 microM) induced 3H-arachidonic acid release and reactive oxygen species (ROS) production via cytosolic phospholipase A2 (cPLA2) activation.
87	20435073	AGE-BSA increased binding of NKA to the alpha-adaptin but not beta2- or mu2-adaptin subunits of the AP-2 clathrin pit adaptor complex.
88	20435073	AGEs may stimulate PIP5Kgamma to increase PIP2 production, which may enhance AP-2 localisation to clathrin pits, increase clathrin pit formation, enhance NKA cargo recognition by AP-2 and/or stimulate cPLA2alpha activity.
89	20435073	AGE-BSA (40 microM) induced 3H-arachidonic acid release and reactive oxygen species (ROS) production via cytosolic phospholipase A2 (cPLA2) activation.
90	20435073	AGE-BSA increased binding of NKA to the alpha-adaptin but not beta2- or mu2-adaptin subunits of the AP-2 clathrin pit adaptor complex.
91	20435073	AGEs may stimulate PIP5Kgamma to increase PIP2 production, which may enhance AP-2 localisation to clathrin pits, increase clathrin pit formation, enhance NKA cargo recognition by AP-2 and/or stimulate cPLA2alpha activity.
92	20838378	Indeed we demonstrate that LPI is able to induce calcium mobilization and activation of Akt and extracellular signal-regulated kinase (ERK)1/2 in these cells and that both pharmacological blockade of GPR55 and its downregulation using specific small interfering RNA strongly inhibits these processes.
93	20838378	We further identify an autocrine loop by which LPI is synthesized by cytosolic phospholipase A2, pumped out of the cell by the ATP-binding cassette transporter ABCC1/MRP1, and is then able to initialize cascades downstream of GPR55.
94	23670971	Induction of cytosolic phospholipase a2α is required for adipose neutrophil infiltration and hepatic insulin resistance early in the course of high-fat feeding.
95	23670971	In the current study, we set out to explore whether adipose tissue infiltration by neutrophils that occurs early (3 days) after initiating a high-fat diet (HFD) could contribute to the early occurrence of hepatic insulin resistance and to determine the role of cytosolic phospholipase A2α (cPLA2α) in this process.
96	23670971	Adipose tissue secretion of tumor necrosis factor-α (TNF-α) was increased by the 3-day HFD, but not if mice were treated with AS or ICAM-1 antibodies.
97	23670971	Induction of cytosolic phospholipase a2α is required for adipose neutrophil infiltration and hepatic insulin resistance early in the course of high-fat feeding.
98	23670971	In the current study, we set out to explore whether adipose tissue infiltration by neutrophils that occurs early (3 days) after initiating a high-fat diet (HFD) could contribute to the early occurrence of hepatic insulin resistance and to determine the role of cytosolic phospholipase A2α (cPLA2α) in this process.
99	23670971	Adipose tissue secretion of tumor necrosis factor-α (TNF-α) was increased by the 3-day HFD, but not if mice were treated with AS or ICAM-1 antibodies.