Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The HPA-1 platelet antigenic system (PLA/Zw) is involved in most cases of antiplatelet alloimmunization. The two alleles HPA-1a and HPA-1b are likely to differ only at the amino acid position 33. This difference is probably due to a unique mutation at base pair position 196 on the glycoprotein IIIa gene which encoded this antigen. Anti HPA-1a alloimmunization is responsible for neonatal thrombocytopenia and post-transfusion purpura. Most immunized women belong to the HLA DR3, DRw52a phenotype, suggesting that this class II molecule may play a role in the presentation of HPA-1a peptide to specific helper T cells.
 ...
PMID:[Anti PLA or anti HPA-1 platelet allo-immunization]. 183 35

Platelets serve as a site for assembly of the proteins of the plasminogen activator system. Once bound to the platelet surface, tissue-type plasminogen activator manifests enhanced catalytic activity. Plasmin, once formed, also binds to the platelets surface and, at low concentrations, renders the platelet dysfunctional by cleaving glycoprotein IIIa selectively in the presence of bound fibrinogen. At higher concentrations (approximately 1 caseinolytic unit/ml), plasmin activates the platelet directly. Activated platelets also bind plasminogen and tissue-type plasminogen activator, and manifest enhanced catalytic efficiency of plasminogen activation. These observations suggest that plasminogen activation by tissue-type plasminogen activator is an autocatalytic process on the platelet surface, and that unique reciprocating mechanisms govern the interaction between platelets and the components of the plasminogen activator system.
 ...
PMID:Platelets and plasminogen activation. 857 74

Fibrinogen is the major ligand of platelet glycoprotein IIb/IIIa platelet receptor. Genes coding for platelet fibrinogen receptor glycoprotein IIb/IIIa are polymorphic. The PLA alloantigen has two antigenic determinants, PLA1 and PLA2, located in a 17-23 kD fragment of glycoprotein IIIa. We analyzed whether PLA genotype has any effect on plasma fibrinogen concentration and investigated if the effect has different magnitude in myocardial infarction patients compared with subjects free of angina or myocardial infarction. One hundred sixteen consecutive patients who suffered a myocardial infarction and 136 subjects recruited by random sampling from the local census were included in the study. PLA genotype distribution and allele frequencies in patients did not significantly differ from those in the control group. Mean fibrinogen concentration tended to be higher in controls with genotype PLA1PLA1 than in those with genotype PLA1PLA2 or PLA2PLA2, and in patients this difference reached statistical significance (p < 0.001). We conclude that the PLA polymorphism may be in linkage disequilibrium with another functional mutation in or near the promoter area of the fibrinogen gene or even in another gene, which controls the production or the clearance of fibrinogen.
 ...
PMID:Platelet glycoprotein IIb/IIIa genetic polymorphism is associated with plasma fibrinogen levels in myocardial infarction patients. The REGICOR Investigators. 987 97

Greenland Inuit are a population with a low risk of cardiovascular disease. Recently, we stated that frequencies of potentially high risk alleles of the apolipoproteins, fibrinogen, factor V, glycoprotein IIIa and factor VII (FVII) genes have different allele frequencies in the Inuit when compared with Caucasian populations. We have extended this study and evaluated whether or not this was also true for the genetic polymorphisms of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), angiotensin-converting enzyme (ACE) and angiotensinogen in a group of 133 Greenland Inuit, aged 30-34 gamma. In addition, we compared the plasma levels of these factors and those of C-reactive protein (CRP) and D-Dimer in Inuit and in Danes, comparable for age and gender. Frequencies (f) were assessed of the alleles that are known as the potential high risk alleles in Caucasians. In the Inuit, the f(insertion allele) of the t-PA intron8ins311 polymorphism was 0.37 (CI 0.32-0.43), the f(4G allele) of the PAI-1 promoter polymorphism was 0.88 (CI 0.83-0.91), the f(deletion allele) of the ACE intron16ins287 polymorphism was 0.40 (CI 0.33-0.47) and the f(M-allele) of the angiotensinogen M/T353 polymorphism was 0.30(CI 0.25-0.38). As for fibrinogen and FVII polymorphisms, these frequencies are all significantly different from what is reported for Caucasian populations. In the Inuit, plasma levels of fibrinogen and D-Dimer were higher than in the Danes, the PAI-1 levels were lower and FVII, t-PA and CRP levels were comparable. The observed allele frequencies of the polymorphisms of t-PA, fibrinogen, FVII, ACE, angiotensinogen and the plasma levels of PAI-1 and D-Dimer were in accordance with the low CVD risk in the Inuit, considering the observed associations between these measures and CVD risk in Caucasian populations, but for other measures this was not the case (allele frequencies of the PAI-1 polymorphism, and plasma levels of fibrinogen, FVII and t-PA). In conclusion there are clear differences in genetic background and plasma levels of risk factors in Greenland Inuit compared with Caucasian populations, and these differences were sometimes, but not always, in accordance with the observed low cardiovascular disease risk of the Inuit population.
 ...
PMID:DNA-polymorphisms and plasma levels of vascular disease risk factors in Greenland Inuit--is there a relation with the low risk of cardiovascular disease in the Inuit? 1023 37