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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.
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 (show PLA2G2A Proteins)-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.
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 (show THSD7A Proteins) antigen expression, screening for circulating anti-podocytes antibodies, and assessment for secondary causes, especially cancer, in patients with THSD7A (show THSD7A Proteins) 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 (show THSD7A Proteins)) 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 (show YWHAZ Proteins) receptor (anti-PLA2R) and anti-THSD7A (show THSD7A Proteins) (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 (show SRPK1 Proteins) proteins and hence resembles a typical inactivating mutation.
Single-nucleotide polymorphism in PLA2R1 gene is associated with primary membranous nephropathy.
blocking the ERRalpha (show ESRRA Proteins)-controlled mitochondrial program largely inhibits the PLA2R1-induced tumor-suppressive response. Together, our data document ERRalpha (show ESRRA Proteins) and its mitochondrial program as downstream effectors of the PLA2R1-JAK2 (show JAK2 Proteins) 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.
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.
180 kDa secretory phospholipase A2 receptor
, M-type receptor
, PLA2-I receptor
, phospholipase A2, group IB, pancreas, receptor
, secretory phospholipase A2 receptor
, yolk sac IgY receptor
, phospholipase A2 receptor 1, 180kDa
, secretory phospholipase A2 receptor-like
, mannose receptor, C type 2
, C-type lectin domain family 13 member C