ArticleDevelopmental cell2017
Amplification of F-Actin Disassembly and Cellular Repulsion by Growth Factor Signaling.
Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed.
- Abl kinase activation promotes axon initial segment disassembly and protein sorting defects in Alzheimer's disease.BMC biology · 2026Article
- Cytokine-Induced Barrier Dysfunction and Lipid Signaling in a Gut-On-Chip Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Structural basis of MICAL autoinhibition.Nature communications · 2024Article
- Disassembly of bundled F-actin and cellular remodeling via an interplay of Mical, cofilin, and F-actin crosslinkers.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- MICALL2 as a substrate of ubiquitinase TRIM21 regulates tumorigenesis of colorectal cancer.Cell communication and signaling : CCS · 2022Article
- Post-Translational Modifications During Brain Development.Advances in experimental medicine and biology · 2022Article
- Phosphorylation of MICAL2 by ARG promotes head and neck cancer tumorigenesis by regulating skeletal rearrangement.Oncogene · 2022Article
- Profilin and Mical combine to impair F-actin assembly and promote disassembly and remodeling.Nature communications · 2021Article
- Propagation of F-actin disassembly via Myosin15-Mical interactions.Science advances · 2021Article
- Enhanced Production of the Mical Redox Domain for Enzymology and F-actin Disassembly Assays.International journal of molecular sciences · 2021Article
- MICAL1 constrains cardiac stress responses and protects against disease by oxidizing CaMKII.The Journal of clinical investigation · 2020Article
- Regulation of actin isoforms in cellular and developmental processes.Seminars in cell & developmental biology · 2020Review
- The receptor tyrosine kinase EPHB6 regulates catecholamine exocytosis in adrenal gland chromaffin cells.The Journal of biological chemistry · 2020Article
- Doublecortin undergo nucleocytoplasmic transport via the RanGTPase signaling to promote glioma progression.Cell communication and signaling : CCS · 2020Article
- Human MICAL1: Activation by the small GTPase Rab8 and small-angle X-ray scattering studies on the oligomerization state of MICAL1 and its complex with Rab8.Protein science : a publication of the Protein Society · 2019Article
- Axon formation, extension, and navigation: only a neuroscience phenomenon?Current opinion in neurobiology · 2018Review
- The MICALs are a Family of F-actin Dismantling Oxidoreductases Conserved from Drosophila to Humans.Scientific reports · 2018Article
- Common effects of attractive and repulsive signaling: Further analysis of Mical-mediated F-actin disassembly and regulation by Abl.Communicative & integrative biology · 2018Article
- MICAL redox enzymes and actin remodeling: New links to classical tumorigenic and cancer pathways.Molecular & cellular oncology · 2018Article
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5 authors.
Funding
Abstract
Extracellular cues that regulate cellular shape, motility, and navigation are generally classified as growth promoting (i.e., growth factors/chemoattractants and attractive guidance cues) or growth preventing (i.e., repellents and inhibitors). Yet, these designations are often based on complex assays and undefined signaling pathways and thus may misrepresent direct roles of specific cues. Here, we find that a recognized growth-promoting signaling pathway amplifies the F-actin disassembly and repulsive effects of a growth-preventing pathway. Focusing on Semaphorin/Plexin repulsion, we identified an interaction between the F-actin-disassembly enzyme Mical and the Abl tyrosine kinase. Biochemical assays revealed Abl phosphorylates Mical to directly amplify Mical Redox-mediated F-actin disassembly. Genetic assays revealed that Abl allows growth factors and Semaphorin/Plexin repellents to combinatorially increase Mical-mediated F-actin disassembly, cellular remodeling, and repulsive axon guidance. Similar roles for Mical in growth factor/Abl-related cancer cell behaviors further revealed contexts in which characterized positive effectors of growth/guidance stimulate such negative cellular effects as F-actin disassembly/repulsion.
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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.