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PLA2R binds to annexinA2-S100A10 (A2t) complex with specific high affinity to the S100A10 component.
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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.
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Suggest strong genetic association between nonsynonymous SNP rs35771982 (p.His300Asp) within PLA2R1 and idiopathic membranous nephropathy.
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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
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Five SNPs around the PLA2R1 gene were significantly associated with idiopathic membranous nephropathy.
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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 .
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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
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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.
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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.
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Single-nucleotide polymorphism in PLA2R1 gene is associated with primary membranous nephropathy.
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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.
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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.
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analysis of Japanese patients reveals that anti-PLA2R antibodies are present in idiopathic membranous nephropathy but not in secondary membranous nephropathy
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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.
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PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation.
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circulating anti-PLA2R antibodies are specific for primary membranous nephropathy.
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PLA2R gene polymorphism is Associated with Increased Intima-Media Thickness of the Carotid Artery.
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Report both serum and kidney levels of PLA2R1 autoantibody in idiopathic membranous nephropathy.
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Pre-transplant phospholipase A2 receptor autoantibody concentration is associated with clinically significant recurrence of membranous nephropathy post-kidney transplantation.
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genetic polymorphism is associated with systemic lupus erythematosus and lupus nephritis in a Chinese patients
