ArticleCell reports. Medicine2025
A genome-wide association study identified PRKCB as a causal gene and therapeutic target for Mycobacterium avium complex disease.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Genetic Susceptibility to Impaired Lung Function in Underground Coal Miners from Kazakhstan.Genes · 2026Article
- Article
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- Article
- Predictive Value of Nutritional Status in Sputum Culture Conversion Among Patients with Nontuberculous Mycobacterial Pulmonary Disease: A Retrospective Cohort Study.Infection and drug resistance · 2026Article
- Genetic Susceptibility to Nontuberculous Mycobacterial Pulmonary Disease: Is It the Chicken or the Egg?American journal of respiratory and critical care medicine · 2025Article
- Integrative molecular network analysis of genetic risk factors to infer biomarkers and therapeutic targets for rheumatoid arthritis.PloS one · 2025Article
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Authors and funding
25 authors.
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Abstract
Non-tuberculous mycobacterial pulmonary disease (NTM-PD) is a chronic progressive lung disease that is increasing in incidence. Host genetic factors are associated with NTM-PD susceptibility. However, the heritability of NTM-PD is not well understood. Here, we perform a two-stage genome-wide association study (GWAS) and discover a susceptibility locus at 16p21 associated with NTM-PD, especially with pulmonary Mycobacterium avium complex (MAC) disease. As the lead variant, rs194800 C allele augments protein kinase C beta (PRKCB) gene expression and associates with severer NTM-PD. The functional studies show that PRKCB exacerbates M. avium infection and promotes intracellular survival of M. avium in macrophages by inhibiting phagosomal acidification. Mechanistically, PRKCB interacts with subunit G of the vacuolar-H
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