ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Loss of modifier of cell adhesion reveals a pathway leading to axonal degeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- DOCKopathies: A systematic review of the clinical pathologies associated with human DOCK pathogenic variants.Human mutation · 2022Pooled it
- Whole-genome bisulfite sequencing of cell-free DNA unveils age-dependent and ALS-associated methylation alterations.Cell & bioscience · 2025Article
- The role of small GTPases in Alzheimer's disease tau pathologies.Frontiers in cellular neuroscience · 2025Review
- Heterozygous loss-of-function variants in DOCK4 cause neurodevelopmental delay and microcephaly.Human genetics · 2024Article
- 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
- DOCK3 regulates normal skeletal muscle regeneration and glucose metabolism.bioRxiv : the preprint server for biology · 2023Article
- An arrayed genome-wide perturbation screen identifies the ribonucleoprotein Hnrnpk as rate-limiting for prion propagation.The EMBO journal · 2022Article
- Integrative analysis of mutated genes and mutational processes reveals novel mutational biomarkers in colorectal cancer.BMC bioinformatics · 2022Article
- Schwannoma Gene Therapy via Adeno-Associated Viral Vector Delivery of Apoptosis-Associated Speck-like Protein Containing CARD (ASC): Preclinical Efficacy and Safety.International journal of molecular sciences · 2022Article
- The p21-activated kinases in neural cytoskeletal remodeling and related neurological disorders.Protein & cell · 2022Review
- Consequences of exposure to pollutants on respiratory health: From genetic correlations to causal relationships.PloS one · 2022Article
- The DOCK protein family in vascular development and disease.Angiogenesis · 2021Review
- Article
- DOCK3 is a dosage-sensitive regulator of skeletal muscle and Duchenne muscular dystrophy-associated pathologies.Human molecular genetics · 2020Article
- Schwannoma gene therapy by adeno-associated virus delivery of the pore-forming protein Gasdermin-D.Cancer gene therapy · 2019Article
- Variants in DOCK3 cause developmental delay and hypotonia.European journal of human genetics : EJHG · 2019Article
- DOCK3-related neurodevelopmental syndrome: Biallelic intragenic deletion of DOCK3 in a boy with developmental delay and hypotonia.American journal of medical genetics. Part A · 2018Article
- The relationship between DNA methylation andOncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Axonal dysfunction is the major phenotypic change in many neurodegenerative diseases, but the processes underlying this impairment are not clear. Modifier of cell adhesion (MOCA) is a presenilin binding protein that functions as a guanine nucleotide exchange factor for Rac1. The loss of MOCA in mice leads to axonal degeneration and causes sensorimotor impairments by decreasing cofilin phosphorylation and altering its upstream signaling partners LIM kinase and p21-activated kinase, an enzyme directly downstream of Rac1. The dystrophic axons found in MOCA-deficient mice are associated with abnormal aggregates of neurofilament protein, the disorganization of the axonal cytoskeleton, and the accumulation of autophagic vacuoles and polyubiquitinated proteins. Furthermore, MOCA deficiency causes an alteration in the actin cytoskeleton and the formation of cofilin-containing rod-like structures. The dystrophic axons show functional abnormalities, including impaired axonal transport. These findings demonstrate that MOCA is required for maintaining the functional integrity of axons and define a model for the steps leading to axonal degeneration.
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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.