ArticleMolecular biology of the cell2011
Splice variant-specific cellular function of the formin INF2 in maintenance of Golgi architecture.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 90 citations in OpenAlex.
- Phosphorylation-dependent interaction between VAP proteins and INF2 influences ER morphology.Current biology : CB · 2026Article
- Regulation of CFTR stability at the plasma membrane-Mechanisms and therapeutic opportunities in cystic fibrosis.FEBS letters · 2026Review
- Regulation of the formin INF2 by actin monomers and calcium/calmodulin.The Journal of cell biology · 2026Article
- Structural and functional dissection of the WH2/DAD motif of INF2, a formin linked to human inherited degenerative disorders.The FEBS journal · 2026Article
- 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
- SUN2 mediates calcium-triggered nuclear actin polymerization to cluster active RNA polymerase II.EMBO reports · 2024Article
- Altered Endoplasmic Reticulum Integrity and Organelle Interactions in Living Cells Expressing INF2 Variants.International journal of molecular sciences · 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
- Activated Drp1 Initiates the Formation of Endoplasmic Reticulum-Mitochondrial Contacts via Shrm4-Mediated Actin Bundling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Structure and function of the N-terminal extension of the formin INF2.Cellular and molecular life sciences : CMLS · 2022Article
- INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury.Nature communications · 2022Article
- Myosin II proteins are required for organization of calcium-induced actin networks upstream of mitochondrial division.Molecular biology of the cell · 2022Article
- Shielding of actin by the endoplasmic reticulum impacts nuclear positioning.Nature communications · 2022Article
- Role of formin INF2 in human diseases.Molecular biology reports · 2022Review
- Formin 3 directs dendritic architecture via microtubule regulation and is required for somatosensory nociceptive behavior.Development (Cambridge, England) · 2021Article
- In pancreatic β-cells myosin 1b regulates glucose-stimulated insulin secretion by modulating an early step in insulin granule trafficking from the Golgi.Molecular biology of the cell · 2021Article
- Multiple roles for actin in secretory and endocytic pathways.Current biology : CB · 2021Review
- Review
- Enterovirus 71 Induces INF2 Cleavage via Activated Caspase-2 in Infected RD Cells.Frontiers in microbiology · 2021Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
INF2 is a unique formin that can both polymerize and depolymerize actin filaments. Mutations in INF2 cause the kidney disease focal and segmental glomerulosclerosis. INF2 can be expressed as two C-terminal splice variants: CAAX and non-CAAX. The CAAX isoform contains a C-terminal prenyl group and is tightly bound to endoplasmic reticulum (ER). The localization pattern and cellular function of the non-CAAX isoform have not been studied. Here we find that the two isoforms are expressed in a cell type-dependent manner, with CAAX predominant in 3T3 fibroblasts and non-CAAX predominant in U2OS, HeLa, and Jurkat cells. Although INF2-CAAX is ER localized in an actin-independent manner, INF2-non-CAAX localizes in an actin-dependent meshwork pattern distinct from ER. INF2-non-CAAX is loosely attached to this meshwork, being extracted by brief digitonin treatment. Suppression of INF2-non-CAAX causes fragmentation of the Golgi apparatus. This effect is counteracted by treatment with the actin monomer-sequestering drug latrunculin B. We also find discrete patches of actin filaments in the peri-Golgi region, and these patches are reduced upon INF2 suppression. Our results suggest that the non-CAAX isoform of INF2 serves a distinct cellular function from that of the CAAX isoform.
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