The human serum protein apolipoprotein L1 (APOL1) kills Trypanosoma brucei but not the sleeping sickness agent Trypanosoma rhodesiense. APOL1 C-terminal variants can kill T. rhodesiense but they also induce kidney disease. Given topological and functional differences between intracellular and extracellular APOL1 isoforms, I propose that trypanolysis and kidney disease result from distinct APOL1 activities.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.pt.2021.11.005 | DOI Listing |
Cells
December 2024
Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires (IBMM), Université Libre de Bruxelles, 6041 Gosselies, Belgium.
The mammalian Apolipoprotein-L families (APOLs) contain several isoforms of membrane-interacting proteins, some of which are involved in the control of membrane dynamics (traffic, fission and fusion). Specifically, human APOL1 and APOL3 appear to control membrane remodeling linked to pathogen infection. Through its association with Non-Muscular Myosin-2A (NM2A), APOL1 controls Golgi-derived trafficking of vesicles carrying the lipid scramblase Autophagy-9A (ATG9A).
View Article and Find Full Text PDFAm J Clin Exp Immunol
October 2024
National Clinical Research Center for Kidney Diseases, Jinling Hospital, Medical School of Nanjing University Nanjing 210002, Jiangsu, China.
J Am Soc Nephrol
June 2024
Laboratory of Molecular Parasitology, IBMM, Université Libre de Bruxelles, Brussels, Belgium.
Kidney Med
June 2024
University of California Davis School of Medicine, Division of Nephrology, Sacramento, CA.
Focal segmental glomerulosclerosis (FSGS) defines a distinct histologic pattern observed in kidney tissue that is linked to several distinct underlying causes, all converging on the common factor of podocyte injury. It presents a considerable challenge in terms of classification because of its varied underlying causes and the limited correlation between histopathology and clinical outcomes. Critically, precise nomenclature is key to describe and delineate the pathogenesis, subsequently guiding the selection of suitable and precision therapies.
View Article and Find Full Text PDFJ Am Soc Nephrol
August 2024
Kidney Disease Section, Kidney Diseases Branch, NIDDK, NIH, Bethesda, Maryland.
Key Points: Apolipoprotein L1 (APOL1)-G1 induced kidney disease in the two APOL1 transgenic mouse models, HIV-associated nephropathy and IFN- administration. Glomerular single-nuclear RNA-sequencing identified genes differentially expressed among mice with APOL1-G1 and G0 variants at single-cell resolution.
Background: Apolipoprotein L1 () high-risk variants contribute to kidney disease among individuals with African ancestry.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!