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anti-Mouse (Murine) PLA2R1 Antibodies:
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Human Polyclonal PLA2R1 Primary Antibody for IHC, IHC (p) - ABIN4345962
Debiec, Ronco: PLA2R autoantibodies and PLA2R glomerular deposits in membranous nephropathy. in The New England journal of medicine 2011
Show all 8 Pubmed References
Human Polyclonal PLA2R1 Primary Antibody for WB - ABIN4345961
Silliman, Moore, Zallen, Gonzalez, Johnson, Elzi, Meng, Hanasaki, Ishizaki, Arita, Ao, England, Banerjee: Presence of the M-type sPLA(2) receptor on neutrophils and its role in elastase release and adhesion. in American journal of physiology. Cell physiology 2002
Show all 2 Pubmed References
Human Polyclonal PLA2R1 Primary Antibody for ELISA, IF - ABIN347712
Hoxha, Harendza, Zahner, Panzer, Steinmetz, Fechner, Helmchen, Stahl: An immunofluorescence test for phospholipase-A2-receptor antibodies and its clinical usefulness in patients with membranous glomerulonephritis. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2011
Human Monoclonal PLA2R1 Primary Antibody for CyTOF, ELISA - ABIN4345963
Fresquet, Jowitt, McKenzie, Ball, Randles, Lennon, Brenchley: PLA2R binds to the annexin A2-S100A10 complex in human podocytes. in Scientific reports 2019
PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation.
Study showed that CTLD1-2 as well as the FNII domain of PLA2R were responsible for binding to collagen I and collagen-dependent migration in both mouse and human PLA2R.
PLA2R might play a pathogenic role in myocardial infarction of PLA2R-deficient mice, through impaired healing of the infarcted region.
PLA2R deficiency increased sPLA2-IB and -X levels in the lung through their impaired clearance from the lung, leading to exaggeration of lung inflammation induced by OVA treatment in a murine model.
Human recombinant soluble PLA2R inhibits integrin beta1-mediated cell responses to collagens.
PLA2R binds to annexinA2-S100A10 (A2t) complex with specific high affinity to the S100A10 component.
Compared with non-PLA2R-associated IMN patients in our cohort, PLA2R-associated IMN patients presented with more severe proteinuria and lower remission rates after treatment, with no distinct histological differences.
Suggest strong genetic association between nonsynonymous SNP rs35771982 (p.His300Asp) within PLA2R1 and idiopathic membranous nephropathy.
We propose a revised clinical workup flow for patients with MN that recommends assessment of kidney biopsy for PLA2R1 and THSD7A antigen expression, screening for circulating anti-podocytes antibodies, and assessment for secondary causes, especially cancer, in patients with THSD7A antibodies
Five SNPs around the PLA2R1 gene were significantly associated with idiopathic membranous nephropathy.
Several risk alleles related to the PLA2R1 gene and within the HLA loci have been identified, whereas epitope spreading of PLA2R may predict treatment response. More recently, thrombospondin type 1 domain-containing 7A (THSD7A) antibodies have been discovered in primary membranous nephropathy .
PLA2R may play a role in some adolescent and preteen idiopathic membranous nephropathy patients but may be less frequently associated with idiopathic membranous nephropathy during childhood
Anti-M-type phospholipase A2 receptor (anti-PLA2R) and anti-THSD7A (thrombospondin type-1 domain-containing 7A) were detected only in membranous neurophathy (MN) patient sera and not in controls.
The frameshift mutation detected in the current study would result in premature stops of amino acid synthesis in PLA2R1 and SRPK1 proteins and hence resembles a typical inactivating mutation.
Single-nucleotide polymorphism in PLA2R1 gene is associated with primary membranous nephropathy.
blocking the ERRalpha-controlled mitochondrial program largely inhibits the PLA2R1-induced tumor-suppressive response. Together, our data document ERRalpha and its mitochondrial program as downstream effectors of the PLA2R1-JAK2 pathway leading to oncosuppression.
Assessment of PLA2R autoimmunity is essential for patient management. Combination of PLA2R-Ab and PLA2R-Ag increases diagnosis sensitivity. PLA2R-Ab titer is a biomarker of disease severity at initial assessment, and the kinetics of the antibody are significantly correlated to disease evolution.
analysis of Japanese patients reveals that anti-PLA2R antibodies are present in idiopathic membranous nephropathy but not in secondary membranous nephropathy
Retrospective study to compare the value of serum anti-PLA2R antibody and glomerular PLA2R deposition in reflecting disease activity and renal function in Chinese patients with membranous nephropathy; serum anti-PLA2R antibody is more closely correlated with disease activity and renal function than glomerular PLA2R deposition.
circulating anti-PLA2R antibodies are specific for primary membranous nephropathy.
PLA2R gene polymorphism is Associated with Increased Intima-Media Thickness of the Carotid Artery.
Report both serum and kidney levels of PLA2R1 autoantibody in idiopathic membranous nephropathy.
Pre-transplant phospholipase A2 receptor autoantibody concentration is associated with clinically significant recurrence of membranous nephropathy post-kidney transplantation.
This gene represents a phospholipase A2 receptor. The encoded protein likely exists as both a transmembrane form and a soluble form. The transmembrane receptor may play a role in clearance of phospholipase A2, thereby inhibiting its action. Polymorphisms at this locus have been associated with susceptibility to idiopathic membranous nephropathy. Alternatively spliced transcript variants encoding different isoforms have been identified.
phospholipase A2 receptor 1, 180kDa
, 180 kDa secretory phospholipase A2 receptor
, M-type receptor
, PLA2-I receptor
, phospholipase A2, group IB, pancreas, receptor
, secretory phospholipase A2 receptor
, C-type lectin domain family 13 member C