ArticleAmerican journal of human genetics2013
Identifying Darwinian selection acting on different human APOL1 variants among diverse African populations.
Article in American journal of human genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
67 citing papers in PubMed, 3 syntheses or guidelines pooled it, 104 citations in OpenAlex.
- KidneyGenAfrica multi-cohort Genome-wide association study and polygenic prediction of kidney function in 110,000 Africans.Nature communications · 2026Pooled it
- APOL1 variant alleles associate with reduced risk for opportunistic infections in HIV infection.Communications biology · 2021Pooled it
- Kidney disease in the setting of HIV infection: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.Kidney international · 2018Guideline
- Germline-targeted baboon apolipoprotein L-1 protects mice against African trypanosomes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Molecular Mechanisms of APOL1-Associated Kidney Disease.International journal of molecular sciences · 2026Review
- Unlocking Ethiopia's genomic landscape and its global significance: a call for inclusive genomics research.Human genomics · 2026Review
- Sodium-glucose co-transporter inhibitors for APOL1 kidney disease: A call for studies.International urology and nephrology · 2025Review
- The APOL1 p.N264K variant is co-inherited with the G2 kidney disease risk variant through a proximity recombination event.G3 (Bethesda, Md.) · 2025Article
- Article
- Apolipoprotein L1 (APOL1) renal risk variant-mediated podocyte cytotoxicity depends on African haplotype and surface expression.Scientific reports · 2024Article
- Versatile Detection of Diverse Selective Sweeps with Flex-Sweep.Molecular biology and evolution · 2023Article
- Is there still evolution in the human population?Biologia futura · 2022Review
- APOL1 genotyping via buccal mucosa cell samples to establish risk of kidney disease.BMC nephrology · 2022Article
- Genome-wide polygenic score to predict chronic kidney disease across ancestries.Nature medicine · 2022Article
- The evolving story of apolipoprotein L1 nephropathy: the end of the beginning.Nature reviews. Nephrology · 2022Review
- The genomic signatures of natural selection in admixed human populations.American journal of human genetics · 2022Article
- Genetic Variants ofKidney international reports · 2022Article
- A spatially aware likelihood test to detect sweeps from haplotype distributions.PLoS genetics · 2022Article
- Similarity-Based Analysis of Allele Frequency Distribution among Multiple Populations Identifies Adaptive Genomic Structural Variants.Molecular biology and evolution · 2022Article
- Advances in integrative African genomics.Trends in genetics : TIG · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedAn, Ping [added]; Winkler, Cheryl A [added]
Authors and funding
13 authors at 7 institutions in 5 countries.
Funding
Abstract
Disease susceptibility can arise as a consequence of adaptation to infectious disease. Recent findings have suggested that higher rates of chronic kidney disease (CKD) in individuals with recent African ancestry might be attributed to two risk alleles (G1 and G2) at the serum-resistance-associated (SRA)-interacting-domain-encoding region of APOL1. These two alleles appear to have arisen adaptively, possibly as a result of their protective effects against human African trypanosomiasis (HAT), or African sleeping sickness. In order to explore the distribution of potential functional variation at APOL1, we studied nucleotide variation in 187 individuals across ten geographically and genetically diverse African ethnic groups with exposure to two Trypanosoma brucei subspecies that cause HAT. We observed unusually high levels of nonsynonymous polymorphism in the regions encoding the functional domains that are required for lysing parasites. Whereas allele frequencies of G2 were similar across all populations (3%-8%), the G1 allele was only common in the Yoruba (39%). Additionally, we identified a haplotype (termed G3) that contains a nonsynonymous change at the membrane-addressing-domain-encoding region of APOL1 and is present in all populations except for the Yoruba. Analyses of long-range patterns of linkage disequilibrium indicate evidence of recent selection acting on the G3 haplotype in Fulani from Cameroon. Our results indicate that the G1 and G2 variants in APOL1 are geographically restricted and that there might be other functional variants that could play a role in HAT resistance and CKD risk in African populations.
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