APOH (beta2-glycoprotein I) notes
Biology
- beta2GPI is an abundant plasma glycoprotein of unknown physiological function [PMID:16480936; PMID:32759297]. It is the main antigen in the antiphospholipid syndrome (APS).
- Core: binds anionic phospholipids (major PL-binding site in domain V) PMID:15486070; inhibits contact activation of the intrinsic pathway PMID:4052628.
- Partners:
- LDLR-family LA modules bind domain V PMID:20223219.
- PF4 PMID:19805618; apo(a) kringle IV PMID:9269765; MBL at domains II and IV PMID:32759297.
- Plasminogen: beta2GPI is a cofactor for tPA activation PMID:16480936; plasmin-nicked beta2GPI binds plasminogen kringle 5 and inhibits plasmin generation PMID:14726399.
- Nicked beta2GPI is anti-angiogenic PMID:17872974.
- PMID:222615 and PMID:7417307 have no abstract in the cache, only titles. Rows from them are kept as non-core with title quotes.
GOA calls
- Protein binding:
- Plasminogen and apo(a) → MODIFY to kringle domain binding.
- PF4 → chemokine binding.
- LDLR and mouse Lrp8 → LDL particle receptor binding.
- MBL → REMOVE: no term fits binding a lectin at a non-carbohydrate site.
- Y2H screen hits (LAMP2, SH3GLB1) → REMOVE.
- Intrinsic coagulation (IDA) → MODIFY to negative regulation of the intrinsic pathway.
- Positive regulation of coagulation (TAS) → over-annotated: the pro-thrombotic effect is the antibodies'.
- Triglyceride transport (IDA/ISS) → over-annotated: the evidence is clearance and LPL activation.
- Lipid binding → MODIFY to lipoprotein particle binding.
- Non-core: LPL rows, lipoprotein particle CC rows, fibrinolysis, plasminogen activation, anti-angiogenic, anti-apoptotic.
- Review round (PR #4160):
- GO:0030195 → MODIFY to GO:2000267 (its is_a descendant, same finding).
- Platelet dense granule → UNDECIDED.
- Lrp8 → GO:0070325.
- PMID:25081279 (thrombosis variant with less anticoagulant capacity) added as support.