ArticleProceedings of the National Academy of Sciences of the United States of America2010
Dock3 induces axonal outgrowth by stimulating membrane recruitment of the WAVE complex.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 86 citations in OpenAlex.
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Sequestration of growth cone surface proteins by cytoplasmic Lrrtm2 inducesbioRxiv : the preprint server for biology · 2026Article
- Alternative pre-mRNA Splicing and Gene Expression Patterns in Midbrain Lineage Cells Carrying Familial Parkinson's Disease Mutations.bioRxiv : the preprint server for biology · 2025Article
- Role of HAUS7 as a DOCK3 binding partner in facilitating axon regeneration.Science advances · 2025Article
- The WAVE complex in developmental and adulthood brain disorders.Experimental & molecular medicine · 2025Review
- Fibrosis and Src Signalling in Glaucoma: From Molecular Pathways to Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Review
- DOCK3 regulates normal skeletal muscle regeneration and glucose metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Neuroprotection and axon regeneration by novel low-molecular-weight compounds through the modification of DOCK3 conformation.Cell death discovery · 2023Article
- Vision protection and robust axon regeneration in glaucoma models by membrane-associated Trk receptors.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- DOCK3 regulates normal skeletal muscle regeneration and glucose metabolism.bioRxiv : the preprint server for biology · 2023Article
- Axonal Regeneration: Underlying Molecular Mechanisms and Potential Therapeutic Targets.Biomedicines · 2022Review
- Fat2 polarizes the WAVE complex ineLife · 2022Article
- TSG-6 released from adipose stem cells-derived small extracellular vesicle protects against spinal cord ischemia reperfusion injury by inhibiting endoplasmic reticulum stress.Stem cell research & therapy · 2022Article
- Musical practice and BDNF plasma levels as a potential marker of synaptic plasticity: an instrument of rehabilitative processes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- DOCK3 is a dosage-sensitive regulator of skeletal muscle and Duchenne muscular dystrophy-associated pathologies.Human molecular genetics · 2020Article
- Strategies to Promote Long-Distance Optic Nerve Regeneration.Frontiers in cellular neuroscience · 2020Article
- DOCK8 is expressed in microglia, and it regulates microglial activity during neurodegeneration in murine disease models.The Journal of biological chemistry · 2019Article
- Variants in DOCK3 cause developmental delay and hypotonia.European journal of human genetics : EJHG · 2019Article
- Redox Pioneer: Professor Hideo Kimura.Antioxidants & redox signaling · 2019Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atypical Rho-guanine nucleotide exchange factors (Rho-GEFs) that contain Dock homology regions (DHR-1 and DHR-2) are expressed in a variety of tissues; however, their functions and mechanisms of action remain unclear. We identify key conserved amino acids in the DHR-2 domain that are critical for the catalytic activity of Dock-GEFs (Dock1-4). We further demonstrate that Dock-GEFs directly associate with WASP family verprolin-homologous (WAVE) proteins through the DHR-1 domain. Brain-derived neurotrophic factor (BDNF)-TrkB signaling recruits the Dock3/WAVE1 complex to the plasma membrane, whereupon Dock3 activates Rac and dissociates from the WAVE complex in a phosphorylation-dependent manner. BDNF induces axonal sprouting through Dock-dependent Rac activation, and adult transgenic mice overexpressing Dock3 exhibit enhanced optic nerve regeneration after injury without affecting WAVE expression levels. Our results highlight a unique mechanism through which Dock-GEFs achieve spatial and temporal restriction of WAVE signaling, and identify Dock-GEF activity as a potential therapeutic target for axonal regeneration.
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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.