The pseudogene encodes a truncated 51-amino acid protein that is homologous to the MBLA isoform in rodents and some primates.

Both the frequency of structural mutations and the promoter polymorphisms that are in strong linkage disequilibrium vary among ethnic groups resulting in seven major haplotypes: HYPA, LYQA, LYPA, LXPA, LYPB, LYQC and HYPD.

While in Golgi, it undergoes two distinct posttranslational modifications and is assembled into high molecular weight multimeric complexes.

[15] MBL belongs to the class of collectins in the C-type lectin superfamily, whose function appears to be pattern recognition in the first line of defense in the pre-immune host.

MBL recognizes carbohydrate patterns found on the surface of a large number of pathogenic micro-organisms, including bacteria, viruses, protozoa and fungi.

MBL binds to carbohydrates (to be specific, D-mannose and L-fucose residues) found on the surfaces of many pathogens.

The subsequent complement cascade catalyzed by C3-convertase results in creating a membrane attack complex, which causes lysis of the pathogen as well as altered-self in the context of apoptotic and necrotic cells.

[25] The three structural polymorphisms of exon 1 have been reported to cause susceptibility to various common infections, including meningococcal disease.