Laboratory for Molecular Diagnostics
Center for Nephrology and Metabolic Disorders

Resistance to trypanosoma brucei

A genetic variation identified in the APOL1 gene causes an increased susceptibility to FSGS but at the same time it helps heterozygous carriers to defend against trypanosoma brucei infections.

Systematic

Hereditary susceptibility to infections
Disorders of mRNA editing
HIV resistance
Malaria
Measles infection susceptibility
Meningococcal infection susceptibility
Resistance to trypanosoma brucei
APOL1
Septic shock

References:

1.

Duchateau PN et al. (2001) Apolipoprotein L gene family: tissue-specific expression, splicing, promoter regions; discovery of a new gene.

[^]
2.

Page NM et al. (2001) The human apolipoprotein L gene cluster: identification, classification, and sites of distribution.

[^]
3.

Mimmack ML et al. (2002) Gene expression analysis in schizophrenia: reproducible up-regulation of several members of the apolipoprotein L family located in a high-susceptibility locus for schizophrenia on chromosome 22.

[^]
4.

Monajemi H et al. (2002) The apolipoprotein L gene cluster has emerged recently in evolution and is expressed in human vascular tissue.

[^]
5.

Vanhamme L et al. (2003) Apolipoprotein L-I is the trypanosome lytic factor of human serum.

[^]
6.

Pérez-Morga D et al. (2005) Apolipoprotein L-I promotes trypanosome lysis by forming pores in lysosomal membranes.

[^]
7.

Genovese G et al. (2010) Association of trypanolytic ApoL1 variants with kidney disease in African Americans.

[^]
8.

Duchateau PN et al. (1997) Apolipoprotein L, a new human high density lipoprotein apolipoprotein expressed by the pancreas. Identification, cloning, characterization, and plasma distribution of apolipoprotein L.

[^]
9.

OMIM.ORG article

Omim 603743 [^]
Update: April 29, 2019