Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of humoral autoimmunity in virus-induced vascular thrombosis is still not clear. We encountered a patient who experienced cerebral ischemia in his early course of Japanese encephalitis. At the beginning, an increase of blood immunoglobulin G isotype of anti-beta2-glycoprotein I antibody, a prolonged activated partial thromboplastin time and thrombocytopenia resembling antiphospholipid antibody syndrome were found, and these abnormalities disappeared when the patient recovered later. A molecular mimicry between the T(2688)LRVLE in Japanese encephalitis virus and hexapeptide-TLRVYK may contribute for the patient's anti-beta2-glycoprotein I antibody generation. Therefore, an increase of procoagulative antibody, such as anti-beta2-glycoprotein I antibody, may display a crucial role for cerebral thrombosis associated with infectious pathogens such as Japanese encephalitis virus. The interaction between autoimmunity induction by infectious agents and procoagulation in the occurrence of vascular thrombosis may be more important than has been understood in previous studies.
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PMID:An increase of blood anti-beta2-glycoprotein I antibody in Japanese encephalitis associated with cerebral ischemia. 1565 May 47

Different proteins, even without sequence similarity, still can contain similar surface regions involved in protein-protein interactions with common target. These regions can serve as structural determinants of cross-reactivity and molecular mimicry. Molecular mimicry, defined as the process in which structural properties of one molecule are simulated by the dissimilar molecules, is implicated in several biologically important processes, including autoimmune and allergic reactions, binding of some ligands to common receptor, and interactions in cell signaling. The problem of identification of the determinants of molecular mimicry is not completely solved at this time. We hypothesize that identification of structurally and chemically similar surface regions of two protein molecules capable of binding to the same target will allow us to identify sites involved in cross-reactivity including determinants of the molecular mimicry. We used a graph-theoretical approach in order to determine highly similar surface regions of two proteins with known three-dimensional structures. This approach uses a variation of Maximal Common Subgraph (MCS) isomorphism, where an association graph is constructed based on the surface-exposed residues of the two molecules and the matching regions are found based on the maximum cliques in the association graph. Testing the proposed method on the targets of autoantibody involved in antiphopholipid syndrome (APS)--beta2-GPI, PC, thrombin, factor IX, factor X, and plasmin allowed identifying potential epitopes for antibody that can inhibit coagulation proteases. Application of this method to the Activated Protein C and factor VII Gla-domains revealed surface regions involved in EPCR and plasma membrane binding, consistent with known experimental results. Analysis of major pollen allergen that can cause food allergies through cross-reactivity found known epitopes involved in cross-reactivity and also revealed additional surface regions that can complement the list of epitopes. Taken together, our results suggest that the proposed graph-theoretical approach can identify determinants of cross-reactivity and molecular mimicry.
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PMID:Graph-theoretical comparison of protein surfaces reveals potential determinants of cross-reactivity and the molecular mimicry. 1993 50

Catastrophic antiphospholipid (Asherson's) syndrome (CAPS) is known to be a severe variant (1%) of antiphospholipid syndrome, with a high rate of mortality (50%). The distinguishing feature of CAPS is microvascular thromboses in the presence of antiphospholipid antibodies. Molecular mimicry between beta2-glycoprotein I and infectious agents, endothelial cell activation and reduced fibrinolysis are the most frequently described pathophysiological mechanisms. Genetic risk factors have also been implicated in the onset of CAPS, although these have not yet been identified. There have been no randomized, controlled trials evaluating the efficacy of any medication on CAPS; however, when CAPS is suspected, aggressive multimodal treatment is required. Patients who receive a combination of anticoagulation therapy, glucocorticosteroids and plasma exchange with or without intravenous immunoglobulin show the best survival rates. Herein, we review the clinical and laboratory findings, diagnostic criteria, pathophysiology, treatment and prognosis of CAPS.
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PMID:Current knowledge regarding Asherson's syndrome. 2047 44