ArticleAmerican journal of physiology. Renal physiology2019
Forward genetic screen in human podocytes identifies diphthamide biosynthesis genes as regulators of adhesion.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 9 citations in OpenAlex.
- DNAJC24 suppresses breast cancer malignancy and serves as a prognostic biomarker.Cancer cell international · 2025Article
- Loss of Diphthamide Increases DNA Replication Stress in Mammalian Cells by Modulating the Translation of RRM1.ACS central science · 2024Article
- Article
- Actin Cytoskeleton and Integrin Components Are Interdependent for Slit Diaphragm Maintenance inCells · 2024Article
- Genetic influences on motor learning and performance and superperforming mutants revealed by random mutational survey of the mouse genome.The Journal of physiology · 2024Article
- UsingFrontiers in cell and developmental biology · 2022Review
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Authors and funding
12 authors at 5 institutions in 3 countries.
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Abstract
Podocyte function is tightly linked to the complex organization of its cytoskeleton and adhesion to the underlying glomerular basement membrane. Adhesion of cultured podocytes to a variety of substrates is reported to correlate with podocyte health. To identify novel genes that are important for podocyte function, we designed an in vitro genetic screen based on podocyte adhesion to plates coated with either fibronectin or soluble Fms-like tyrosine kinase-1 (sFLT1)/Fc. A genome-scale pooled RNA interference screen on immortalized human podocytes identified 77 genes that increased adhesion to fibronectin, 101 genes that increased adhesion to sFLT1/Fc, and 44 genes that increased adhesion to both substrates when knocked down. Multiple shRNAs against diphthamide biosynthesis protein 1-4 (DPH1-DPH4) were top hits for increased adhesion. Immortalized human podocyte cells stably expressing these hairpins displayed increased adhesion to both substrates. We then used CRISPR-Cas9 to generate podocyte knockout cells for
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