Parcial analysis of factor I gene in two deficient sisters of this protein (1999)
- Authors:
- Autor USP: ISAAC, LOURDES - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Imprenta:
- Publisher: Brazilian Society for Immunology
- Publisher place: Águas de Lindóia
- Date published: 1999
- Source:
- Título: Summary
- Conference titles: Annual Meeting of the Brazilian Society for Immunology
-
ABNT
BARACHO, G. V. et al. Parcial analysis of factor I gene in two deficient sisters of this protein. 1999, Anais.. Águas de Lindóia: Brazilian Society for Immunology, 1999. . Acesso em: 01 jan. 2026. -
APA
Baracho, G. V., Bastos, W., Nudelman, V., & Isaac, L. (1999). Parcial analysis of factor I gene in two deficient sisters of this protein. In Summary. Águas de Lindóia: Brazilian Society for Immunology. -
NLM
Baracho GV, Bastos W, Nudelman V, Isaac L. Parcial analysis of factor I gene in two deficient sisters of this protein. Summary. 1999 ;[citado 2026 jan. 01 ] -
Vancouver
Baracho GV, Bastos W, Nudelman V, Isaac L. Parcial analysis of factor I gene in two deficient sisters of this protein. Summary. 1999 ;[citado 2026 jan. 01 ] - Ultrastructural aspects of alpha - 2 - macroglobulin activited mouse macrophages
- A hereditary human complement C3 deficiency due reduced C3 mRNA
- Molecular caracterization of factor I deficency in two brazilian sisters
- Deficiency of factor I is present in two sisters from a family with low levels of factor H
- Um novo caso de deficiência de C3 do sistema complemento humano
- Immunological characterization of a human C3 deficiency
- Inherited complete factor I deficiency associated with systemic lupus enythematosus, higher susceptibility to infection and low levels of factor H
- Concentrations of regulatory complement proteins in Brazilian Nealthy children and adults
- Alpha-2-macroglobulin enhances complement and igg mediated phagocytosis by mouse macrophages
- A new model of outbred genetically selected mice which present strong acute inflammatory response and Nramp-1 resistant gene in the absence of C5
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