Ignet

Gene Information

Gene symbol: PLA2G1B

Gene name: phospholipase A2, group IB (pancreas)

HGNC ID: 9030

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKR1B1	1 hits
3	AKT1	1 hits
4	ALB	1 hits
5	C5AR1	1 hits
6	COL1A1	1 hits
7	HAVCR1	1 hits
8	INF2	1 hits
9	LRP2	1 hits
10	MME	1 hits
11	NELL1	1 hits
12	NPHS1	1 hits
13	PIK3CA	1 hits
14	PLA2G2A	1 hits
15	PLA2G6	1 hits
16	PLA2R1	1 hits
17	PLCB1	1 hits
18	PLCG1	1 hits
19	SOD1	1 hits
20	SOD2	1 hits
21	THBS1	1 hits
22	THSD7A	1 hits
23	TRPC6	1 hits

Related Sentences

#	PMID	Sentence
1	35276323	The antigen responsible for 70-80% of IMN is a podocyte protein called M-type phospholipase A2 receptor (PLA2R).
2	35220046	In membranous nephropathy (MN), measurement of serum circulating autoantibodies against podocyte transmembrane glycoprotein M-type phospholipase A2 receptor (PLA2R) and thrombospondin type 1 domain-containing 7A (THSD7A), immunohistochemical staining of kidney tissue for glomerular PLA2R, THSD7A, neural epidermal growth factor-like 1 protein (NELL-1) and specific types of immunoglobulin G (IgG) may be useful adjuncts when screening for underlying malignancies.
3	34899763	The identification of the major target antigen phospholipase A2 receptor (PLA2R) in the majority of primary (idiopathic) cases of membranous nephropathy (MN) has been followed by the rapid identification of numerous minor antigens that appear to define phenotypically distinct forms of disease.
4	34707715	Significantly increased urinary and renal KIM-1 levels were observed in the nonremission with IST group compared with those in the spontaneous remission group, and the same trend was observed for the plasma anti-podocyte antigen phospholipase A2 receptor antibody levels.
5	34707715	Urinary and renal KIM-1 levels were positively correlated with blood urea nitrogen, serum creatinine, serum cystatin-C, urinary albumin/creatinine ratio, urinary β2-microglobulin and the renal interstitial fibrosis index, and they were negatively correlated with serum albumin.
6	34700229	Rapamycin attenuates PLA2R activation-mediated podocyte apoptosis via the PI3K/AKT/mTOR pathway.
7	34700229	Rapamycin attenuates PLA2R activation-mediated podocyte apoptosis via the PI3K/AKT/mTOR pathway.
8	34700229	Primary MN has been associated with circulating antibodies against native podocyte antigens, including phospholipase A2 receptor (PLA2R); however, precision therapy targeting the signaling cascade of PLA2R activation is lacking.
9	34700229	Primary MN has been associated with circulating antibodies against native podocyte antigens, including phospholipase A2 receptor (PLA2R); however, precision therapy targeting the signaling cascade of PLA2R activation is lacking.
10	34700229	We demonstrated that podocyte apoptosis was induced by Group IB secretory phospholipase A2 (sPLA2IB) in a concentration- and time-dependent manner via upregulation of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mTOR, and inhibited by rapamycin or LY294002.
11	34700229	We demonstrated that podocyte apoptosis was induced by Group IB secretory phospholipase A2 (sPLA2IB) in a concentration- and time-dependent manner via upregulation of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mTOR, and inhibited by rapamycin or LY294002.
12	34700229	Furthermore, aberrant activation of the PI3K/AKT/mTOR pathway triggers both extrinsic (caspase-8 and caspase-3) and intrinsic (Bcl-2-associated X protein [BAX], B-cell lymphoma 2 [BCL-2], cytochrome c, caspase-9, and caspase-3) apoptotic cascades in podocytes.
13	34700229	Furthermore, aberrant activation of the PI3K/AKT/mTOR pathway triggers both extrinsic (caspase-8 and caspase-3) and intrinsic (Bcl-2-associated X protein [BAX], B-cell lymphoma 2 [BCL-2], cytochrome c, caspase-9, and caspase-3) apoptotic cascades in podocytes.
14	34700229	The therapeutic implications of our findings are that strategies to reduce PLA2R activation and PI3K/AKT/mTOR pathway inhibition in PLA2R-activated podocytes help protect podocytes from apoptosis.
15	34700229	The therapeutic implications of our findings are that strategies to reduce PLA2R activation and PI3K/AKT/mTOR pathway inhibition in PLA2R-activated podocytes help protect podocytes from apoptosis.
16	34337081	A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy.
17	34337081	Membranous nephropathy (MN) is an organ-restricted autoimmune disease mainly caused by circulating autoantibodies against podocyte antigens, including the M-type phospholipase A2 receptor (PLA2R) and thrombospondin domain-containing 7A (THSD7A).
18	34337081	Antibodies against PLA2R are present in 70%-80% and against THSD7A in 2% of adult patients, which provides a paradigm shift in molecular diagnosis and management monitoring.
19	34160953	The auto-immune nature of the disease was confirmed in the last decade with the discovery of a growing list of podocyte antigens targeted by autoantibodies, e.g. phospholipase A2 receptor (PLA2R).
20	33910688	Autoantibodies directed against the M-type phospholipase A2 receptor (PLA2R) and thrombospondin 1 domain-containing 7 A (THSD7A) can be used as diagnostic biomarkers.
21	33910688	Recently, further antigens like NELL-1 (neural tissue encoding protein with EGF-like repeats-1), exostosin 1 and 2 have been discovered.
22	33808418	The clinical management of MN has steadily advanced owing to the identification of autoantibodies to the phospholipase A2 receptor (PLA2R) in 2009 and thrombospondin domain-containing 7A (THSD7A) in 2014 on the podocyte surface.
23	33808418	Additionally, evidence is emerging that NELL-1 is associated with 5-10% of PMN cases that are PLA2R- and THSD7A-negative, which moves us one step closer to mapping out the full spectrum of PMN antigens.
24	33808418	Recent developments suggest exostosin 1 (EXT1), EXT2, NELL-1, and contactin 1 (CNTN1) are associated with MN.
25	33351779	In most cases, this autoimmune kidney disease is associated with autoantibodies against the M-type phospholipase A2 receptor (PLA2R1) expressed on kidney podocytes, but the mechanisms leading to glomerular damage remain elusive.
26	33351779	Here, we developed a cell culture model using human podocytes and found that anti-PLA2R1-positive pMN patient sera or isolated IgG4, but not IgG4-depleted sera, induced proteolysis of the 2 essential podocyte proteins synaptopodin and NEPH1 in the presence of complement, resulting in perturbations of the podocyte cytoskeleton.
27	33351779	Specific blockade of the lectin pathway prevented degradation of synaptopodin and NEPH1.
28	33351779	Assembly of the terminal C5b-9 complement complex and activation of the complement receptors C3aR1 or C5aR1 were required to induce proteolysis of synaptopodin and NEPH1 by 2 distinct proteolytic pathways mediated by cysteine and aspartic proteinases, respectively.
29	33346502	Since the moment of animal model creation and the recognition of podocytes damage as a key mechanism of MN development, the identification of antigens, first of all the phospholipase A2 receptor (PLA2R), and the development of methods of PLA2R autoantibodies detection and its monitoring opened a new era in the idiopathic MN (iMN) diagnosis, treatment and prognosis evaluation.
30	33184968	Secretory phospholipase A2 group IB (sPLA2-IB) and M-type phospholipase A2 receptor (PLA2R) are closely associated with proteinuria in idiopathic membranous nephropathy (IMN).
31	33184968	In vitro sPLA2-IB-induced insufficient autophagy in podocytes and promoted podocyte injury via activation of the mTOR/ULK1^ser757 signaling pathway.
32	33042109	Several auto-antigens have recently been identified in IMN, including M-type receptor for secretory phospholipase A2 (PLA2R1), thrombospondin type-1 domain-containing 7A (THSD7A), and neural epidermal growth factor-like 1 protein (NELL-1).
33	33042109	Induced by environmental stimuli or other causes, the PLA2R1 antigen and/or THSD7A antigen exposed to extrarenal tissues, such as lungs, then produce the auto-antibodies that target and cause damage to the podocytes in circulation.
34	32862379	Antibody against M-type receptor for secretory phospholipase A2 (PLA2R1) was positive in 81.3% IMN patients.
35	32712166	Downstream mechanisms that lead to podocyte injury following phospholipase A2 receptor (PLA2R) autoimmunity remain elusive.
36	32712166	To help define this we compared urinary metabolomic profiles of patients with PLA2R-associated membranous nephropathy (MN) at the time of kidney biopsy with those of patients with minimal change disease (MCD) and to healthy individuals.
37	32712166	Among the metabolites differentially expressed in patients with PLA2R-associated MN compared to healthy individuals, fumarate was the only significant differentially expressed metabolite in PLA2R-associated MN compared to MCD [fold-difference vs. healthy controls and vs.
38	32712166	Fumarate hydratase, which hydrolyzes fumarate, colocalized with podocalyxin, and its expression was lower in glomerular sections from patients with PLA2R-associated MN than in those from healthy individuals, patients with non-PLA2R-associated MN or MCD.
39	32712166	These changes were coupled to alterations in the expression of molecules involved in the phenotypic profile of podocytes (WT1, ZO-1, Snail, and fibronectin), an increase in albumin flux across the podocyte layer and the production of reactive oxygen species in podocytes.
40	32664235	Tacrolimus Prevents TWEAK-Induced PLA2R Expression in Cultured Human Podocytes.
41	32664235	Primary membranous nephropathy is usually caused by antibodies against the podocyte antigen membrane M-type phospholipase A2 receptor (PLA2R).
42	32664235	We have now identified key TNF receptor superfamily members in podocytes and explored the regulation of PLA2R expression and the impact of tacrolimus.
43	32664235	Data mining of single cell transcriptomics and glomerular transcriptomics data identified TNFRSF12a/Fn14 as the highest expressed TNF receptor superfamily gene in human membranous nephropathy, and this was confirmed by immunohistochemistry that also identified NFκB activation in membranous nephropathy podocytes.
44	32664235	Furthermore, in cultured human podocytes, TWEAK increased the expression of PLA2R as well as the expression of other genes recently identified by GWAS as linked to membranous nephropathy: NFKB1 and IRF4.
45	32664235	Interestingly, IRF4 encodes the FK506-binding protein 52 (FKBP52), a protein associated with tacrolimus.
46	32664235	Tacrolimus prevented the increased expression of PLA2R, NFKB1 and IRF4 induced by TWEAK in cultured podocytes.
47	32083137	The phospholipase A2 receptor (PLA2R1) is the major autoantigen in idiopathic membranous nephropathy (MN).
48	32061439	Over the last decade important research discoveries have revealed that most "idiopathic" cases are caused by autoantibodies to podocyte antigens including phospholipase A2 receptor (PLA2R) and thrombospondin type 1 domain containing 7A (THSD7A).
49	31998325	Membranous Nephropathy (MN) is an autoimmune disease associated with antibodies against podocyte proteins: M-type phospholipase A2 receptor (PLA2R1) or thrombospondin type-1 domain-containing 7A (THSD7A) in 70 and 3% of patients, respectively.
50	31611068	The discovery in 2009 of the M-type phospholipase A2 receptor (PLA2R) as the primary target in membranous nephropathy (MN) greatly advanced basic and clinical research.
51	31610191	Idiopathic membranous nephropathy (IMN) has recently attracted much attention due to the development of auto antibodies, anti-phospholipase A2 receptor and anti-thrombospondin type I domain-containing 7A on podocytes, the establishment of immune networks complexes in circulation as well as the development of autoreactive immune cells against kidney, in both innate and adaptive participants.
52	31610191	In addition, altered B cell signaling network by the B cell receptor and co receptors such as B cell-activating factor receptor (BAFFR) stimulates the autoimmune-related pathogenesis.
53	31447839	In idiopathic membranous nephropathy (IMN) the immune complexes are formed by circulating antibodies binding mainly to one of two naturally-expressed podocyte antigens: the M-type receptor for secretory phospholipase A2 (PLA2R1) and the Thrombospondin type-1 domain-containing 7A (THSD7A).
54	31336376	The discovery of -autoantibodies against the podocyte-expressed M-type phospholipase A2 receptor (PLA2R) provided a clear pathophysiological rationale for interventions targeting the B-cell lineage to prevent antibody production and subepithelial immune-complex deposition.
55	31244861	Anti-phospholipase A2 receptor (PLA2R) autoantibodies are detected in 70-80% of patients.
56	30639075	The relationship of anti-phospholipase A2 receptor antibody and C5a complement with disease activity and short-term outcome in idiopathic membranous nephropathy.
57	30538665	The presence of autoantibodies against podocyte antigens phospholipase A2 receptor (PLA2R) and thrombospondin type 1 domain containing 7A (THSD7A) in MN suggests an autoimmune mechanism.
58	30538665	Some CIDP patients also harbor autoantibodies against paranodal proteins such as neurofascin 155 (NF155) and contactin-1 (CNTN1).
59	30394845	MiR-130a-5p prevents angiotensin II-induced podocyte apoptosis by modulating M-type phospholipase A2 receptor.
60	30394845	MiR-130a-5p prevents angiotensin II-induced podocyte apoptosis by modulating M-type phospholipase A2 receptor.
61	30394845	We compared the renal expressions of miR-130a-5p and M-type phospholipase A2 receptor (PLA2R) between MN patients (n = 30) and 30 controls by qRT-PCR and western blot, respectively.
62	30394845	We compared the renal expressions of miR-130a-5p and M-type phospholipase A2 receptor (PLA2R) between MN patients (n = 30) and 30 controls by qRT-PCR and western blot, respectively.
63	30394845	Interaction between miR-130a-5p and PLA2R was determined using dual-luciferase reporter gene assay.
64	30394845	Interaction between miR-130a-5p and PLA2R was determined using dual-luciferase reporter gene assay.
65	29104026	In addition to functioning as an enzyme, PLA₂ can activate a phospholipase A2 receptor (PLA2R1) in plasma membrane.
66	29104026	While the list of PLA₂ targets extends to glucose homeostasis, intracellular energy balance, adipocyte development, and hepatic lipogenesis, the PLA2R1 downstream effectors are few and scarcely investigated.
67	29104026	PLA2R1 was shown to induce activation of Janus-kinase 2 (JAK2) and estrogen-related receptor α (ERRα)-controlled mitochondrial proteins, as well as increasing the accumulation of reactive oxygen species, thus leading to apoptosis and senescence.
68	28904430	Immunohistochemical (IHC) evaluation with the help of anti-phospholipase A2 receptor (PLA2R) antibody helps in tissue evaluation of iMN, which is an easy, cost-effective, and pathologist-friendly technique.
69	28674044	PLA2R and THSD7A: Disparate Paths to the Same Disease?
70	28674044	The phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A) are the two major autoantigens in primary membranous nephropathy (MN), and define two molecular subclasses of this disease.
71	28674044	PLA2R-associated MN was initially found to associate with risk alleles within HLA-DQA1, but subsequent studies have shifted the focus to the HLA-DRB locus.
72	28674044	Although protocols similar to those that identified PLA2R and THSD7A may be successful in the identification of novel antigenic targets in MN, newer techniques such as laser-capture mass spectrometry or protein arrays may be helpful as well.
73	28669992	The discovery of nephritogenic autoantibodies against podocyte M-type phospholipase A2 receptor (PLA₂R) and thrombospondin type-1 domain- containing protein 7A (THSD7A) antigens provides a clear pathophysiological rationale for interventions that specifically target B-cell lineages to prevent antibody production and subepithelial deposition.
74	28577748	In 2009, the M-type phospholipase A2 receptor (PLA2R), a podocyte membrane glycoprotein, was identified as the first autoantigen involved in more than 70 % of primitive membranous nephropathy.
75	28065518	The autoimmune nature of IMN was clearly delineated in 2009 with the identification of the glomerular-deposited IgG to be a podocyte receptor, phospholipase A2 receptor (PLA2R) in 70% to 75% of cases.
76	28065518	Immunostaining of biopsy specimens has further detected either PLA2R or THSD7A antigen in the deposited immune complexes in 5% to 10% of cases autoantibody seronegative at the time of biopsy.
77	27631233	Idiopathic membranous nephropathy (IMN) is known to be associated with antibodies acting on the M-type phospholipase A2 receptor (PLA2R) of the podocyte.
78	27226532	Genetic Ablation of Calcium-independent Phospholipase A2γ Induces Glomerular Injury in Mice.
79	27226532	Genetic Ablation of Calcium-independent Phospholipase A2γ Induces Glomerular Injury in Mice.
80	27226532	We reported previously that calcium-independent phospholipase A2γ (iPLA2γ) is cytoprotective against complement-mediated glomerular epithelial cell injury.
81	27226532	We reported previously that calcium-independent phospholipase A2γ (iPLA2γ) is cytoprotective against complement-mediated glomerular epithelial cell injury.
82	27199983	In primary MN, autoantibodies target proteins expressed on the podocyte surface, often phospholipase A2 receptor (PLA2R1).
83	26854253	Phospholipase A2 receptor (PLA2R) expressed in human podocytes has been highlighted as a causative autoantigen of human idiopathic membranous nephropathy.
84	26854253	The cultured cells expressed PLA2R mRNA and protein in addition to other podocyte markers (synaptopodin, podocin and nephrin).
85	26597209	It shows how experimental models developed more than 30 years ago have led to the identification of several human antigens including neutral endopeptidase in the neonate, phospholipase A2 receptor, and thrombospondin 1 domain 7A in the adult, and cationic bovine serum albumin in children.
86	26459770	The M-type phospholipase A2 receptor (PLA2R) has been identified as the main target antigen, as it can be found in approximately 70% of iMN patients but only rarely in other glomerulonephritides.
87	26459770	A genetic background for iMN has been demonstrated by genome-wide association studies that have shown highly significant associations of the PLA2R1 and the human leucocyte antigen (HLA)-DQA1 loci with iMN.
88	26400544	It was discovered in 2009 that phospholipase A2 receptor (PLA2R), a normal transmembrane protein in podocyte plasma membrane, is the antigen causing MGN.
89	26372979	The neutral endopeptidase (NEP) and the receptor for secretory phospholipase A2 (PLA2R) have been identified as target antigens for circulating and deposited antibodies in allo-immune neonatal and adult " idiopathic " MN, respectively.
90	26372979	In Europeans, genome-wide studies have shown an association between alleles of PLA2R1 and HLA DQA1 (class II genes of tissue histocompatibility complex) genes and idiopathic MN.
91	26090644	In 2002, podocyte neutral endopeptidase was identified as an antigenic target of circulating antibodies in alloimmune neonatal nephropathy, and in 2009, podocyte phospholipase A2 receptor (PLA2R) was reported as an antigenic target in autoimmune adult membranous nephropathy.
92	25997506	The majority of cases of primary membranous nephropathy (MN) are associated with auto-antibodies against the podocyte antigen M-type phospholipase A2 receptor (PLA2R).
93	25335547	sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor.
94	25335547	sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor.
95	25335547	sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor.
96	25335547	The M-type phospholipase A2 receptor (PLA2R) is expressed in podocytes in human glomeruli.
97	25335547	The M-type phospholipase A2 receptor (PLA2R) is expressed in podocytes in human glomeruli.
98	25335547	The M-type phospholipase A2 receptor (PLA2R) is expressed in podocytes in human glomeruli.
99	25335547	Group IB secretory phospholipase A2 (sPLA2 IB), which is one of the ligands of the PLA2R, is more highly expressed in chronic renal failure patients than in controls.
100	25335547	Group IB secretory phospholipase A2 (sPLA2 IB), which is one of the ligands of the PLA2R, is more highly expressed in chronic renal failure patients than in controls.
101	25335547	Group IB secretory phospholipase A2 (sPLA2 IB), which is one of the ligands of the PLA2R, is more highly expressed in chronic renal failure patients than in controls.
102	25335547	However, the roles of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are unknown.
103	25335547	However, the roles of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are unknown.
104	25335547	However, the roles of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are unknown.
105	25335547	In the present study, we found that more podocyte apoptosis occurs in the kidneys of patients with higher PLA2R and serum sPLA2 IB levels.
106	25335547	In the present study, we found that more podocyte apoptosis occurs in the kidneys of patients with higher PLA2R and serum sPLA2 IB levels.
107	25335547	In the present study, we found that more podocyte apoptosis occurs in the kidneys of patients with higher PLA2R and serum sPLA2 IB levels.
108	25335547	After binding with the PLA2R, sPLA2 IB induced podocyte apoptosis in a time- and concentration-dependent manner. sPLA2 IB-induced podocyte PLA2R upregulation was not only associated with increased ERK1/2 and cPLA2α phosphorylation but also displayed enhanced apoptosis.
109	25335547	After binding with the PLA2R, sPLA2 IB induced podocyte apoptosis in a time- and concentration-dependent manner. sPLA2 IB-induced podocyte PLA2R upregulation was not only associated with increased ERK1/2 and cPLA2α phosphorylation but also displayed enhanced apoptosis.
110	25335547	After binding with the PLA2R, sPLA2 IB induced podocyte apoptosis in a time- and concentration-dependent manner. sPLA2 IB-induced podocyte PLA2R upregulation was not only associated with increased ERK1/2 and cPLA2α phosphorylation but also displayed enhanced apoptosis.
111	25335547	In contrast, PLA2R-silenced human podocytes displayed attenuated apoptosis. sPLA2 IB enhanced podocyte arachidonic acid (AA) content in a dose-dependent manner.
112	25335547	In contrast, PLA2R-silenced human podocytes displayed attenuated apoptosis. sPLA2 IB enhanced podocyte arachidonic acid (AA) content in a dose-dependent manner.
113	25335547	In contrast, PLA2R-silenced human podocytes displayed attenuated apoptosis. sPLA2 IB enhanced podocyte arachidonic acid (AA) content in a dose-dependent manner.
114	25335547	These data indicate that sPLA2 IB has the potential to induce human podocyte apoptosis via binding to the PLA2R.
115	25335547	These data indicate that sPLA2 IB has the potential to induce human podocyte apoptosis via binding to the PLA2R.
116	25335547	These data indicate that sPLA2 IB has the potential to induce human podocyte apoptosis via binding to the PLA2R.
117	25335547	The sPLA2 IB-PLA2R interaction stimulated podocyte apoptosis through activating ERK1/2 and cPLA2α and through increasing the podocyte AA content.
118	25335547	The sPLA2 IB-PLA2R interaction stimulated podocyte apoptosis through activating ERK1/2 and cPLA2α and through increasing the podocyte AA content.
119	25335547	The sPLA2 IB-PLA2R interaction stimulated podocyte apoptosis through activating ERK1/2 and cPLA2α and through increasing the podocyte AA content.
120	25187357	PLA2R-associated membranous glomerulopathy is modulated by common variants in PLA2R1 and HLA-DQA1 genes.
121	25187357	Membranous glomerulopathy (MG) is most commonly caused by autoantibodies directed against the podocyte phospholipase A2 receptor (PLA2R1) and common variants in this gene are associated with MG.
122	25187357	There was strong epistasis between HLA-DQA1 SNP rs2187668 and the PLA2R1 variant rs35771982.
123	25187357	Thus, common variants in the PLA2R1, particularly rs35771982, modulate PLA2R-positive MG with HLA-DQA1 in Caucasians.
124	24990336	These IgG4 antibodies are thought to react with antigens, primarily the phospholipase A2 receptor (PLA2R) expressed on the podocyte cell membrane.
125	24942189	Serum with phospholipase A2 receptor autoantibodies interferes with podocyte adhesion to collagen.
126	24676616	In this setting, the M-type phospholipase A2 receptor (PLA2R) was identified as the first major antigen target in human primary MN.
127	24553432	ATP effects were also abolished by inhibiting G protein signaling and by the PLC/PLA2 inhibitor D-609.
128	24196483	Here we improved ELV isolation protocols employing density centrifugation to remove THP and albumin, and isolated a glomerular membranous vesicle (GMV)-enriched subfraction from 7 individuals identifying 1830 proteins and in 3 patients with glomerular disease identifying 5657 unique proteins.
129	24196483	We show many nephrotic syndrome proteins, proteases, and complement proteins involved in glomerular disease are in GMVs and some were only shed in the disease state (nephrin, TRPC6, INF2 and phospholipase A2 receptor).
130	24161038	Recent studies have identified the M-type phospholipase A2 receptor (PLA2R) as the major target antigen in primary MN.
131	24075959	Recently, studies on the underlying pathomechanisms led to the identification of the podocyte M-type receptor for secretory phospholipase A2 (PLA2R1) as a target antigen of circulating autoantibodies.
132	23689575	The dominant autoantigen is M-type phospholipase A2 receptor protein (PLA2R1) expressed on the surface of native glomerular podocytes.
133	23657570	Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol.
134	23657570	Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes.
135	23657570	Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082).
136	23657570	Podocin and TRPC6 interact at their respective COOH termini.
137	23657570	Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog.
138	23657570	These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation.
139	23657570	They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene.
140	23657570	Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present.
141	23401979	In recent years, first human podocyte autoantigens, responsible for autoantibodies and in situ immune complexes formation, were discovered: neutral endopeptidase, m-type phospholipase A2 receptor, superoxide-dismutase 2, aldose-reductase, alpha-enolase.
142	24594573	Most adult forms of MN are autoimmune diseases without identified etiology (primary MN), linked to the production of antibodies raised against another podocyte antigen, the type-M phospholipase A2 receptor (PLA2R1).
143	21388432	Megalin, NEP and PLA(2) R are all expressed on the podocyte surface, where they can serve as targets for circulating antibodies, leading to in situ immune complex formation, complement activation and proteinuria. 4.
144	20182413	These include identification of neutral endopeptidase (NEP) as the target antigen in alloimmune MN resulting from fetomaternal immunization in NEP-deficient mothers, and our demonstration that a high proportion of patients with idiopathic MN (IMN) have circulating antibodies to the M-type phospholipase A2 receptor (PLA2R), a transmembrane protein located on podocytes.