ArticleKidney international2016
Mice with mutant Inf2 show impaired podocyte and slit diaphragm integrity in response to protamine-induced kidney injury.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Patient-specific hiPSC-Podocytes as an in vitro model of genetic FSGS.Scientific reports · 2025Article
- Autosomal dominant focal segmental glomerulosclerosis by INF2 p.Arg218Trp and p.Ser186Pro mutations: three case reports and literature review.BMC nephrology · 2025Review
- Regulation of formin INF2 and its alteration in INF2-linked inherited disorders.Cellular and molecular life sciences : CMLS · 2024Review
- INF2 mutations cause kidney disease through a gain-of-function mechanism.Science advances · 2024Article
- INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death.Cellular and molecular life sciences : CMLS · 2024Article
- An inactivating human TRPC6 channel mutation without focal segmental glomerulosclerosis.Cellular and molecular life sciences : CMLS · 2023Article
- Bioengineering Strategies to Develop Podocyte Culture Systems.Tissue engineering. Part B, Reviews · 2022Review
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Article
- The glomerular filtration barrier: a structural target for novel kidney therapies.Nature reviews. Drug discovery · 2021Review
- Formins in Human Disease.Cells · 2021Review
- Role of actin cytoskeleton in podocytes.Pediatric nephrology (Berlin, Germany) · 2021Review
- Role of Rho GTPase Interacting Proteins in Subcellular Compartments of Podocytes.International journal of molecular sciences · 2021Review
- Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy.Journal of the American Society of Nephrology : JASN · 2021Article
- The formin INF2 in disease: progress from 10 years of research.Cellular and molecular life sciences : CMLS · 2020Review
- A Deregulated Stress Response Underlies Distinct INF2-Associated Disease Profiles.Journal of the American Society of Nephrology : JASN · 2020Article
- Loss of Roundabout Guidance Receptor 2 (Robo2) in Podocytes Protects Adult Mice from Glomerular Injury by Maintaining Podocyte Foot Process Structure.The American journal of pathology · 2020Article
- FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes.Journal of the American Society of Nephrology : JASN · 2020Article
- Functional importance of an inverted formin C-terminal tail at morphologically dynamic epithelial junctions.Cytoskeleton (Hoboken, N.J.) · 2019Article
- Recruitment of APOL1 kidney disease risk variants to lipid droplets attenuates cell toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Mutations in the INF2 (inverted formin 2) gene, encoding a diaphanous formin family protein that regulates actin cytoskeleton dynamics, cause human focal segmental glomerulosclerosis (FSGS). INF2 interacts directly with certain other mammalian diaphanous formin proteins (mDia) that function as RhoA effector molecules. FSGS-causing INF2 mutations impair these interactions and disrupt the ability of INF2 to regulate Rho/Dia-mediated actin dynamics in vitro. However, the precise mechanisms by which INF2 regulates and INF2 mutations impair glomerular structure and function remain unknown. Here, we characterize an Inf2 R218Q point-mutant (knockin) mouse to help answer these questions. Knockin mice have no significant renal pathology or proteinuria at baseline despite diminished INF2 protein levels. INF2 mutant podocytes do show impaired reversal of protamine sulfate-induced foot process effacement by heparin sulfate perfusion. This is associated with persistent podocyte cytoplasmic aggregation, nephrin phosphorylation, and nephrin and podocin mislocalization, as well as impaired recovery of mDia membrane localization. These changes were partially mimicked in podocyte outgrowth cultures, in which podocytes from knockin mice show altered cellular protrusions compared to those from wild-type mice. Thus, in mice, normal INF2 function is not required for glomerular development but normal INF2 is required for regulation of the actin-based behaviors necessary for response to and/or recovery from injury.
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