ArticleMolecular therapy. Nucleic acids2022
Filamin A pre-mRNA editing modulates vascularization and tumor growth.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular Context of ADAR-Mediated Editing of Coding RNA in Colorectal and Lung Cancers.International journal of molecular sciences · 2026Article
- Integrated heart-blood RNA editome profiling reveals circulating A-to-I editing candidates linked to dilated cardiomyopathy myocardial signatures and heart failure.Journal of molecular and cellular cardiology plus · 2026Article
- Unravelling the Phosphorylation Landscape of Anthrax Toxin Receptor 1: Mechanisms and Functional Insights Through Phosphoproteomic Data Integration.The protein journal · 2025Article
- Filamin A editing in myeloid cells reduces intestinal inflammation and protects from colitis.The Journal of experimental medicine · 2025Article
- FLNA, a disulfidptosis-related gene, modulates tumor immunity and progression in colorectal cancer.Cellular & molecular biology letters · 2025Article
- RNA editing in disease: mechanisms and therapeutic potential.RNA (New York, N.Y.) · 2025Review
- Role of Filamin A in Growth and Migration of Breast Cancer-Review.Current issues in molecular biology · 2024Review
- Recommendations for detection, validation, and evaluation of RNA editing events in cardiovascular and neurological/neurodegenerative diseases.Molecular therapy. Nucleic acids · 2024Review
- RBPs: an RNA editor's choice.Frontiers in molecular biosciences · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine to inosine (A to I) editing is mediated by adenosine deaminases acting on RNA (ADAR) enzymes. Inosines are interpreted as guanosines by the translational machinery. Consequently, A to I editing in mRNAs can lead to their recoding and the formation of proteins not encoded in the genome. Filamin A is an actin-crosslinking protein. A to I editing in the filamin pre-mRNA leads to the exchange of a glutamine to an arginine in a highly interactive domain of the protein. However, the consequences of this editing event are still poorly understood. Here we show, using transgenic mice expressing either constitutively edited or constitutively uneditable filamin A that filamin A editing critically controls angiogenesis in tumors but also in a mouse ischemia model. Hyper-editing reduces angiogenesis, while hypoediting leads to increased angiogenesis, possibly by altering vascular endothelial growth factor receptor 2 (VEGFR2) turnover. Further, FLNA editing of the tumor itself seemingly affects its metastatic potential by changing its interaction with the extracellular matrix. We therefore identify filamin A editing as a critical component for angiogenesis, tumor growth, and metastasis formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.