DIALLELIC POLYMORPHISM MAY EXPLAIN VARIATIONS OF THE BLOOD CONCENTRATION OF MANNAN‐BINDING PROTEIN IN ESKIMOS, BUT NOT IN BLACK AFRICANS

International Journal of Immunogenetics

Volumn 19, Issue 6, 1992, Pages 403-412

  Garred, P ^a   Madsen, H O ^a   Kurtzhals, J A L ^a   Lamm, L U ^a   Thiel, S ^c   Hey, A S ^b   Svejgaard, A ^a  

^a University of Copenhagen   (Denmark)

^b AARHUS UNIVERSITY HOSPITAL   (Denmark)

^c AARHUS UNIVERSITY   (Denmark)

Author keywords

[No Author keywords available]

Indexed keywords

ASPARTIC ACID; BINDING PROTEIN; COMPLEMENT; GLYCINE; LECTIN; MANNAN;

ADOLESCENT; ADULT; ALLELE; AMINO ACID SUBSTITUTION; ARTICLE; CLINICAL ARTICLE; CODON; COMPARATIVE STUDY; CONTROLLED STUDY; EXON; FEMALE; GENE; GENE FREQUENCY; GENETIC POLYMORPHISM; GENOTYPE; GREENLAND; HUMAN; IMMUNE DEFICIENCY; KENYA; MALE; MUTANT; OPSONIZATION; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; RACE DIFFERENCE; RECURRENT INFECTION;

ADOLESCENT; ADULT; ALLELES; BASE SEQUENCE; CARRIER PROTEINS; COLLECTINS; COMPARATIVE STUDY; DNA; ESKIMOS; FEMALE; GENE FREQUENCY; GREENLAND; HUMAN; IMMUNOLOGIC DEFICIENCY SYNDROMES; KENYA; MALE; MANNANS; MIDDLE AGE; MOLECULAR SEQUENCE DATA; MONGOLOID RACE; NEGROID RACE; POLYMORPHISM (GENETICS); SUPPORT, NON-U.S. GOV'T; VARIATION (GENETICS);

EID: 0026453082     PISSN: 17443121     EISSN: 1744313X     Source Type: Journal    
DOI: 10.1111/j.1744-313X.1992.tb00083.x     Document Type: Article

References (34)

1. Molecular biology of G 6 PD variants
2. Human class II major histocompatibility antigen β‐chains are derived from at least three loci
3. Reconstruction of human evolution: Bringing together genetic, archaelogical, and linguistic data
4. Complement deficiencies
5. Complement and infectious agents: A tale of disguise and deception
6. Activation‐dependent antigenic changes of human C3
7. Serum lectin with known structure activates complement through the classical pathway
8. Complement evasion by bacteria and parasites
9. Isolation and characterization of mannan‐binding protein from rabbit liver
10. Study of H‐LA system in Eskimos
11. Populations genetics
12. Frequency of the mutation responsible for mannose binding protein deficiency
13. Identical point mutation leading to low levels of mannose binding protein and poor C3b mediated opsonisation in Chinese and Caucasian populations
14. 2 complex, of the classical pathway of complement, without involvement of Clq
15. Human leukocyte Clq receptor binds other soluble proteins with collagen domains
16. The third component of complement (C3) is responsible for the intracellular survival of Leishmania major
17. Molecular organization and function of the complement system
18. Phagocytosis of Legionella pneumophilia is mediated by human complement receptors
19. The human mannose‐binding protein gene — Exon structure reveals its evolutionary relationship to a human pulmonary surfactant gene and localization to chromosome 10
20. IgA deficiency
21. Phagocytosis of Mycobacterium tuberculosis is mediated by human monocyte complement receptors and complement component C3
22. Inherited complement deficiency states and disease
23. Molecular basis of opsonic defect in immunodeficient children
24. Association of low levels of mannan‐binding protein with a common defect in opsonisation
25. Structure and evolutionary origin of the gene encoding a human serum mannose‐binding protein
26. Structures and functions associated with the group of mammalian lectins containing collagen sequences
27. Deficiency of mannan binding protein — A new complement deficiency syndrome
28. The molecular basis of a common defect in opsonization
29. Clq solid‐phase radioimmunoassay: Binding properties of solid‐phase Clq and evidence that Clq‐bindng IgG complexes in systemic lupus erythematosus are not bound to endogenous Clq
30. Low‐molecular weight Clq‐binding immunoglobulin G in patients with systemic lupus erythematosus consists of autoantibodies to the collagen‐like region of Clq
31. The complement profile in clinical medicine. Inherited and acquired conditions lowering the serum concentrations of complement component and control proteins
32. Maintenance of multiallelic polymorphism at the MHC region