Affinage

DNM2

Dynamin-2 · UniProt P50570

Length
870 aa
Mass
98.1 kDa
Annotated
2026-06-09
48 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DNM2 is a large GTPase that mediates membrane fission across multiple intracellular compartments by acting at the necks of membrane tubules and vesicles [PMID:20711168, PMID:bio_10.1101_2024.12.05.24318153]. It drives scission events in the endolysosomal and autophagic pathways: at late endosomes it forms an EGF-induced complex with the adaptor CIN85 required for late endosomal budding and EGFR downregulation, with loss producing elongated late-endosomal tubules and sustained signaling (PMID:20711168), and it severs recycling endosome tubules to release autophagosome precursors through direct binding to LC3 (PMID:32315611). DNM2 also interacts with Drp1 via its GTPase domain to complete the terminal steps of mitochondrial fission [PMID:bio_10.1101_2024.12.05.24318153]. Its activity is restrained by BIN1 (amphiphysin 2), which inhibits DNM2 GTPase activity and acts as a genetic modifier of DNM2-dependent disease (PMID:40042903). DNM2 is a central pathogenic node in centronuclear myopathy (CNM) and Charcot-Marie-Tooth (CMT) neuropathy: dominant CNM mutations such as R465W and S619L act through gain-of-function hyperactivity and protein mislocalization that impair membrane tubulation, endocytosis, and autophagy (PMID:30925452, PMID:34837441, PMID:24135484, PMID:31691805), and lipid binding through the PH domain — rather than protein level or GTPase activity alone — is the specific molecular function driving CNM pathology downstream of MTM1 loss (PMID:42100875). Reducing DNM2 expression genetically rescues multiple forms of CNM in vivo, establishing elevated or hyperactive DNM2 as the driver of disease (PMID:28589938, PMID:30291191).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2010 High

    Established that DNM2 acts in a regulated, signal-dependent complex at late endosomes, extending its fission role beyond the plasma membrane into endolysosomal trafficking.

    Evidence Reciprocal Co-IP of DNM2 with CIN85, knockdown/dominant-negative experiments with EGFR trafficking and morphology readouts

    PMID:20711168

    Open questions at the time
    • Does not define how DNM2 oligomerization is nucleated at the late endosomal neck
    • Structural basis of the DNM2-CIN85 interaction not resolved
  2. 2013 Medium

    Connected a specific CNM mutation to defective membrane tubulation and excitation-contraction coupling, linking DNM2 dysfunction to muscle pathology in vivo.

    Evidence Zebrafish transgenic expression of DNM2-S619L, COS7 BIN1-dependent tubulation assay, EM and calcium imaging

    PMID:24135484

    Open questions at the time
    • Does not establish whether the tubulation defect reflects gain or loss of function
    • Mechanistic link between vesicular accumulation and EC-coupling defect unresolved
  3. 2013 Low

    Implicated PH domain integrity in proper DNM2 subcellular localization, hinting at the lipid-interaction basis of CNM later confirmed mechanistically.

    Evidence Immunofluorescence of patient muscle biopsy carrying a PH-domain D614N variant, family genetic analysis

    PMID:23374900

    Open questions at the time
    • Single patient/family without mechanistic reconstitution
    • Causality of the variant not demonstrated experimentally
    • No biochemical measurement of altered lipid binding
  4. 2017 High

    Demonstrated that lowering DNM2 prevents and reverses myopathy in an MTM1-loss model, defining elevated DNM2 as a pathogenic driver downstream of MTM1 and a therapeutic target.

    Evidence Systemic antisense oligonucleotide knockdown in Mtm1KO mice with histopathology and muscle force readouts

    PMID:28589938

    Open questions at the time
    • Does not identify which DNM2 molecular activity (lipid binding vs GTPase) underlies pathology
    • Mechanism connecting MTM1 loss to DNM2 elevation unresolved
  5. 2017 Medium

    Showed DNM2 is co-opted into a leukemic survival complex, broadening its role to endocytosis-linked signaling in disease beyond muscle.

    Evidence Co-IP with SH3/proline-rich domain mapping of an AHI-1–BCR-ABL–DNM2 complex, DNM2 knockdown with survival/apoptosis assays in CML cells

    PMID:28366933

    Open questions at the time
    • Direct fission function of DNM2 in this complex not demonstrated
    • Single lab, single cellular context
  6. 2017 Medium

    Identified DNM2 as a phospho-target whose modification drives Golgi remodeling during viral infection, indicating post-translational control of DNM2 function.

    Evidence Western blot for phospho-DNM2 with Src inhibitor (PP2) rescue, IF and TEM of Golgi in HSV-1-infected neurons

    PMID:28879169

    Open questions at the time
    • Direct phosphorylation site on DNM2 not mapped
    • Whether phospho-DNM2 directly mediates Golgi fission unproven
  7. 2018 High

    Established that reducing both WT and mutant DNM2 alleles corrects a dominant gain-of-function myopathy, generalizing DNM2 lowering as a therapeutic strategy.

    Evidence AAV-shRNA and ASO knockdown in Dnm2-R465W/+ knock-in mice with histopathology, ultrastructure, and muscle force

    PMID:30291191

    Open questions at the time
    • Therapeutic window for safe DNM2 reduction not defined
    • Does not isolate the mutant-specific molecular defect
  8. 2019 Medium

    Confirmed at the allele level that R465W is a gain-of-function mutation defective in two specific DNM2-dependent processes, endocytosis and autophagy.

    Evidence Allele-specific CRISPR/Cas9 correction in patient fibroblasts and mouse myoblasts, transferrin uptake and autophagy flux assays

    PMID:30925452

    Open questions at the time
    • Does not link the in vitro cellular defects to the in vivo muscle phenotype quantitatively
    • Mechanism of gain-of-function at the molecular level not resolved here
  9. 2019 Medium

    Visualized that CNM mutations cause DNM2 mislocalization and aggregation in living muscle, providing an in vivo correlate of disease-associated mislocalization.

    Evidence Transgenic zebrafish live imaging comparing WT and mutant DNM2 with motor and ultrastructural phenotyping

    PMID:31691805

    Open questions at the time
    • Does not establish whether aggregation is cause or consequence of dysfunction
    • Molecular trigger of mutant aggregation unknown
  10. 2020 High

    Defined a mechanistic route by which a CNM mutation impairs autophagy: R465W mis-partners with ITSN1 at the plasma membrane, depleting DNM2 from LC3-dependent autophagosome formation sites.

    Evidence Co-IP of DNM2 with LC3 and ITSN1, autophagy flux assays, CNM mutant expression and imaging

    PMID:32315611

    Open questions at the time
    • Stoichiometry of DNM2 redistribution between membranes not quantified
    • Whether LC3 binding directly templates fission unresolved
  11. 2021 Medium

    Linked the magnitude of DNM2 GTPase hyperactivity to in cellulo membrane defects and clinical severity, supporting hyperactivity as the unifying mechanism of CNM mutations.

    Evidence In cellulo T-tubule-like structure assay across multiple variants correlated with biochemical GTPase activity and clinical phenotype

    PMID:34837441

    Open questions at the time
    • Correlation does not prove GTPase activity alone is the pathogenic determinant
    • Does not separate GTPase from lipid-binding contributions
  12. 2023 Medium

    Revealed that DNM2 abundance is set by ubiquitin-proteasome turnover and is pharmacologically tunable, offering a non-genetic route to lower elevated DNM2.

    Evidence Tamoxifen treatment of BIN1-CNM and DNM2-CNM mice with Western blot for DNM2, cullin 3 and p62, transcriptomics, and contractility

    PMID:36562127

    Open questions at the time
    • Direct ubiquitination of DNM2 by a cullin-3 ligase not demonstrated
    • Mechanism connecting tamoxifen to cullin 3 normalization unresolved
  13. 2024 Medium

    Extended DNM2 fission function to mitochondria, showing GTPase-domain-dependent interaction with Drp1 completes mitochondrial division and controls cell-cycle progression.

    Evidence Co-IP with domain mapping, super-resolution colocalization at fission sites, RNA-seq and flow cytometry after DNM2 silencing in pulmonary arterial smooth muscle cells (preprint)

    PMID:bio_10.1101_2024.12.05.24318153

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Whether DNM2 is obligatory for mitochondrial fission in other cell types unclear
  14. 2025 High

    Established BIN1 as a direct biochemical inhibitor of DNM2 GTPase activity and an in vivo genetic modifier of DNM2-driven disease severity.

    Evidence In vitro GTPase assay with BIN1 plus genetic epistasis (Dnm2-K562E/+ × Bin1+/−) with motor, histological, and integrin readouts

    PMID:40042903

    Open questions at the time
    • Structural mechanism of BIN1-mediated GTPase inhibition not resolved
    • Does not address regulation of DNM2 by BIN1 in non-muscle tissues
  15. 2026 High

    Pinpointed PH-domain lipid binding, rather than protein level or GTPase activity per se, as the specific molecular function driving CNM pathology downstream of MTM1 loss.

    Evidence AAV delivery of WT and mutant DNM2 (including lipid-binding-defective K562E) in Mtm1-/y mice with survival, force, fiber sizing, organelle positioning, and genetic epistasis

    PMID:42100875

    Open questions at the time
    • Does not define the specific lipid species or membrane site driving pathology
    • Relationship between lipid binding and the GTPase-hyperactivity model not fully reconciled
  16. 2026 Medium

    Demonstrated that DNM2 augmentation can correct CMT-related muscle defects but only within a narrow dosage window, framing DNM2 level as a tightly balanced determinant of muscle integrity.

    Evidence Muscle-specific transgenic and systemic AAV DNM2 overexpression in Dnm2-K562E/+ mice with histopathology, desmin/integrin IF, and mitochondrial EM

    PMID:41683892

    Open questions at the time
    • Optimal therapeutic dose and timing not defined
    • Mechanism by which excess DNM2 produces CNM-like features not dissected

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DNM2's distinct molecular activities (lipid binding, GTPase hydrolysis, oligomerization) are coordinated at each membrane compartment, and how this is tuned to set the narrow tolerable range of DNM2 activity across tissues, remains unresolved.
  • No integrated structural model linking lipid binding, GTPase activity, and fission output
  • Tissue-specific regulators beyond BIN1 and cullin 3 not identified
  • Mechanism unifying CNM gain-of-function GTPase and lipid-binding models unsettled

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 2 GO:0140657 ATP-dependent activity 2 GO:0008289 lipid binding 1
Localization
GO:0005739 mitochondrion 1 GO:0005768 endosome 1 GO:0005794 Golgi apparatus 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 2 R-HSA-9612973 Autophagy 2 R-HSA-1852241 Organelle biogenesis and maintenance 1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2020 DNM2 mediates scission of recycling endosome tubules to release nascent autophagosome precursors; this process is regulated by DNM2 binding to LC3 and is increased by autophagy-inducing stimuli. The CNM-causing DNM2-R465W mutant is defective in this scission step because it shows increased binding to the plasma membrane partner ITSN1, depleting normal DNM2 from autophagosome formation sites on recycling endosomes. Cell imaging, autophagy flux assays, co-immunoprecipitation of DNM2 with LC3 and ITSN1, expression of CNM mutant DNM2 in cells Developmental cell High 32315611
2010 DNM2 directly interacts with the adaptor protein CIN85 (SH3-domain-containing protein of 85 kDa) in a complex that is induced by EGF receptor stimulation. This DNM2-CIN85 interaction occurs at late endosomes and is required for late endosomal budding/scission; disruption of this interaction results in accumulation of internalized EGFR in aberrantly elongated late endosomal tubules and sustained downstream signaling. Co-immunoprecipitation, dominant-negative and knockdown experiments, live-cell and fluorescence imaging of late endosome morphology, EGFR trafficking assay The EMBO journal High 20711168
2013 Expression of the CNM-causing DNM2-S619L mutation in zebrafish leads to accumulation of aberrant vesicular structures and defective excitation-contraction coupling; in COS7 cells, DNM2-S619L causes defective BIN1-dependent membrane tubule formation, indicating the mutation impairs membrane tubulation. Zebrafish transgenic expression, COS7 cell tubulation assay, electron microscopy, calcium imaging Disease models & mechanisms Medium 24135484
2017 DNM2 interacts with the scaffold protein AHI-1 via the AHI-1 SH3 domain binding to the DNM2 proline-rich domain, forming an AHI-1–BCR-ABL–DNM2 protein complex in CML stem/progenitor cells that regulates leukemic cell survival and TKI resistance through cellular endocytosis and ROS-mediated autophagy. Co-immunoprecipitation, domain-mapping experiments (SH3 and proline-rich domain truncations), DNM2 knockdown with survival/apoptosis assays Leukemia Medium 28366933
2017 HSV-1 neuronal infection triggers Src tyrosine kinase activation and subsequent phosphorylation of Dynamin 2 (DNM2), leading to fragmentation and scattering of the Golgi apparatus; pharmacological inhibition of Src kinase (PP2) markedly reduces these Golgi morphological alterations. HSV-1 tegument protein VP11/12 is necessary but not sufficient for Dyn2 phosphorylation. Immunofluorescence, transmission electron microscopy, pharmacological Src inhibition (PP2), primary neuronal cultures, Western blot for phospho-DNM2 Frontiers in cellular and infection microbiology Medium 28879169
2019 In transgenic zebrafish, wild-type DNM2 shows distinctive subcellular compartmentalization in muscle in vivo; CNM-related DNM2 mutations cause protein mislocalization and aggregation in muscle, whereas wild-type DNM2 does not aggregate. Transgenic zebrafish live imaging, subcellular localization analysis, motor function assays, muscle ultrastructure analysis Human molecular genetics Medium 31691805
2013 A novel DNM2 D614N mutation in the PH domain is associated with profound mislocalization of DNM2 and membrane trafficking proteins (concentrated at centrally located nuclei rather than normal distribution) in patient muscle fibers, without significant change in total DNM2 protein level, causally linking PH domain integrity to proper DNM2 subcellular localization and myofiber organization. Immunofluorescence of patient muscle biopsy, protein expression analysis, genetic analysis of family members Neuromuscular disorders : NMD Low 23374900
2017 Genetic reduction of DNM2 (via antisense oligonucleotides) in Mtm1 knockout mice (a model of X-linked centronuclear myopathy) efficiently reduces DNM2 protein in muscle and prevents myopathy development; ASO injection into severely affected mice reverses muscle pathology within 2 weeks, establishing that elevated DNM2 is a pathogenic driver downstream of MTM1 loss. Antisense oligonucleotide (ASO) systemic delivery in Mtm1KO mice, histopathology, muscle force measurements, Western blot Nature communications High 28589938
2018 Reduction of DNM2 via AAV-shRNA or antisense oligonucleotides in Dnm2-R465W/+ knock-in mice (DNM2-related CNM model) rescues muscle mass, fiber size, histopathology, and ultrastructure, demonstrating that reducing both WT and mutant DNM2 alleles can correct a dominant gain-of-function myopathy. Intramuscular AAV-shRNA injection, systemic ASO delivery, histopathology, muscle force/mass measurements, Western blot Proceedings of the National Academy of Sciences of the United States of America High 30291191
2019 Allele-specific CRISPR/Cas9 inactivation or correction of the heterozygous DNM2-R465W mutation in patient fibroblasts and mouse myoblasts rescues altered transferrin uptake (endocytosis) and autophagy phenotypes, confirming the R465W mutation causes gain-of-function defects in these two DNM2-dependent cellular processes. CRISPR/Cas9 allele-specific editing, transferrin uptake assay, autophagy flux assay in patient and mouse cells Molecular therapy. Nucleic acids Medium 30925452
2025 BIN1 (amphiphysin 2) inhibits the GTPase activity of DNM2; genetic reduction of BIN1 in Dnm2-K562E/+ CMT mice increases the activity of the K562E DNM2 mutant, restores motor performance, ameliorates muscle and nerve structural defects, and normalizes integrin localization in muscle. Conversely, increasing BIN1 exacerbates Dnm2-K562E/+ phenotypes, establishing BIN1 as a modifier of DNM2 activity and disease severity. In vitro GTPase activity assay with BIN1, genetic epistasis (Dnm2K562E/+ × Bin1+/- mice), motor and histological phenotyping, integrin immunofluorescence Proceedings of the National Academy of Sciences of the United States of America High 40042903
2026 DNM2 lipid binding (via PH domain) is the specific molecular function driving CNM pathology: a lipid-binding-defective K562E mutant of DNM2, when expressed in Mtm1-/y mice, fully rescues survival, motor function, muscle force, fiber size, and organelle positioning despite persistently elevated DNM2 protein levels, while GTPase-active or other mutants fail to rescue. This establishes DNM2 lipid binding, not protein level or GTPase activity per se, as the pathogenic driver in MTM1-CNM. AAV-mediated delivery of WT and DNM2 mutants in WT and Mtm1-/y mice, muscle force measurements, histopathology, fiber sizing, organelle positioning; genetic epistasis (Mtm1-/y Dnm2K562E/+ mice) JCI insight High 42100875
2016 DNM2 (dynamin 2) is required for efficient Japanese encephalitis virus (JEV) replication; siRNA knockdown of DNM2 in PK15 cells significantly reduces JEV replication, identifying DNM2-dependent vesicle scission as a host factor exploited by JEV for cellular entry/replication. siRNA knockdown of DNM2, viral replication assay (JEV), miR-124 overexpression with DNM2 target validation Virology journal Low 27329300
2023 Tamoxifen reduces the abnormally elevated DNM2 protein level in both BIN1-CNM and DNM2-CNM mouse models through a mechanism involving normalization of cullin 3 (E3 ubiquitin ligase) protein level, suggesting ubiquitin-proteasome-mediated regulation of DNM2 abundance underlies the therapeutic effect. Tamoxifen dietary treatment in CNM mouse models, Western blot for DNM2 and ubiquitin-proteasome markers (cullin 3, p62), transcriptome analysis, muscle contractility measurements Brain : a journal of neurology Medium 36562127
2024 DNM2 interacts with Drp1 via its GTPase domain, enabling mitochondrial translocation and facilitating the terminal steps of mitochondrial fission; silencing DNM2 in pulmonary arterial smooth muscle cells inhibits mitochondrial fission and causes G1/G0 cell cycle arrest, while DNM2 overexpression accelerates fission and proliferation. RGCC is identified as a downstream cell-cycle effector of this DNM2-Drp1 axis. Co-immunoprecipitation, super-resolution microscopy for colocalization at fission sites, truncated-domain expression constructs, RNA-seq after DNM2 silencing, flow cytometry for cell cycle, siRNA knockdown bioRxivpreprint Medium bio_10.1101_2024.12.05.24318153
2024 DNM2 is recruited to the neck of vacuole-like protrusions (VLPs) formed during Shigella flexneri cell-to-cell spread, dependent on PIK3C3-mediated PtdIns(3)P accumulation, where it mediates membrane scission to resolve protrusions into double-membrane vacuoles. Live-fluorescence confocal microscopy tracking, PIK3C3 inhibition, DNM2 localization imaging at VLP necks during bacterial spread bioRxivpreprint Low bio_10.1101_2024.10.31.621244
2021 Novel DNM2 variants associated with CNM induce gain-of-function phenotypes in a cell-based imaging assay (T-tubule-like structure formation); the degree of impairment in cellulo correlates with biochemical gain-of-function GTPase activity measurements and clinical disease severity, providing evidence that DNM2 CNM mutations act via hyperactivity. In cellulo imaging assay for T-tubule-like structures, biochemical GTPase activity assay for mutant proteins Human mutation Medium 34837441
2026 Muscle-specific DNM2 overexpression in Dnm2-K562E/+ CMT mice ameliorates desmin and integrin mislocalization, membrane trafficking defects, mitochondrial abnormalities, and fibrosis in skeletal muscle independently of nerve involvement. Systemic postnatal AAV-DNM2 delivery paradoxically worsened muscle pathology producing CNM-like features, revealing that precise DNM2 dosage is critical and that the therapeutic window for DNM2 augmentation in muscle is narrow. Tissue-specific transgenic overexpression, AAV systemic delivery, histopathology, immunofluorescence for desmin/integrin, electron microscopy for mitochondria International journal of molecular sciences Medium 41683892

Source papers

Stage 0 corpus · 48 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Phase variation of HpuAB and HmbR, two distinct haemoglobin receptors of Neisseria meningitidis DNM2. Molecular microbiology 89 10361300
2017 Antisense oligonucleotide-mediated Dnm2 knockdown prevents and reverts myotubular myopathy in mice. Nature communications 87 28589938
2010 Expanding the clinical, pathological and MRI phenotype of DNM2-related centronuclear myopathy. Neuromuscular disorders : NMD 80 20227276
2018 Reducing dynamin 2 (DNM2) rescues DNM2-related dominant centronuclear myopathy. Proceedings of the National Academy of Sciences of the United States of America 56 30291191
2006 MRI in DNM2-related centronuclear myopathy: evidence for highly selective muscle involvement. Neuromuscular disorders : NMD 53 17134899
2014 Characterization of dual PTEN and p53-targeting microRNAs identifies microRNA-638/Dnm2 as a two-hit oncogenic locus. Cell reports 49 25088422
2018 Differential Expression of Several miRNAs and the Host Genes AATK and DNM2 in Leukocytes of Sporadic ALS Patients. Frontiers in molecular neuroscience 46 29670510
2020 A DNM2 Centronuclear Myopathy Mutation Reveals a Link between Recycling Endosome Scission and Autophagy. Developmental cell 45 32315611
2010 A Dyn2-CIN85 complex mediates degradative traffic of the EGFR by regulation of late endosomal budding. The EMBO journal 44 20711168
2018 Dynamin 2 (DNM2) as Cause of, and Modifier for, Human Neuromuscular Disease. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 41 30426359
2018 Single Intramuscular Injection of AAV-shRNA Reduces DNM2 and Prevents Myotubular Myopathy in Mice. Molecular therapy : the journal of the American Society of Gene Therapy 40 29506908
2013 The myopathy-causing mutation DNM2-S619L leads to defective tubulation in vitro and in developing zebrafish. Disease models & mechanisms 39 24135484
2012 Multiple recognition motifs in nucleoporin Nup159 provide a stable and rigid Nup159-Dyn2 assembly. The Journal of biological chemistry 37 23223634
2018 Melatonin activates FIS1, DYN1, and DYN2 Plasmodium falciparum related-genes for mitochondria fission: Mitoemerald-GFP as a tool to visualize mitochondria structure. Journal of pineal research 32 29480948
2019 Allele-Specific CRISPR/Cas9 Correction of a Heterozygous DNM2 Mutation Rescues Centronuclear Myopathy Cell Phenotypes. Molecular therapy. Nucleic acids 31 30925452
2009 Centronuclear myopathy with cataracts due to a novel dynamin 2 (DNM2) mutation. Neuromuscular disorders : NMD 31 19932620
2011 Phenotype variability and histopathological findings in centronuclear myopathy due to DNM2 mutations. Journal of neurology 30 21221624
2010 Sporadic centronuclear myopathy with muscle pseudohypertrophy, neutropenia, and necklace fibers due to a DNM2 mutation. Neuromuscular disorders : NMD 28 20817456
2016 Targeting High Dynamin-2 (DNM2) Expression by Restoring Ikaros Function in Acute Lymphoblastic Leukemia. Scientific reports 27 27885263
2019 Insights into wild-type dynamin 2 and the consequences of DNM2 mutations from transgenic zebrafish. Human molecular genetics 25 31691805
2017 A novel AHI-1-BCR-ABL-DNM2 complex regulates leukemic properties of primitive CML cells through enhanced cellular endocytosis and ROS-mediated autophagy. Leukemia 24 28366933
2013 A novel mutation in the DNM2 gene impairs dynamin 2 localization in skeletal muscle of a patient with late onset centronuclear myopathy. Neuromuscular disorders : NMD 22 23374900
2013 The yeast dynein Dyn2-Pac11 complex is a dynein dimerization/processivity factor: structural and single-molecule characterization. Molecular biology of the cell 21 23761070
2017 Herpes Simplex Virus Type 1 Neuronal Infection Perturbs Golgi Apparatus Integrity through Activation of Src Tyrosine Kinase and Dyn-2 GTPase. Frontiers in cellular and infection microbiology 19 28879169
2016 miR-124 attenuates Japanese encephalitis virus replication by targeting DNM2. Virology journal 17 27329300
2023 Tamoxifen improves muscle structure and function of Bin1- and Dnm2-related centronuclear myopathies. Brain : a journal of neurology 14 36562127
2015 DNM2 mutations in a cohort of sporadic patients with centronuclear myopathy. Genetics and molecular biology 11 26273216
2017 Phenotype variability and histopathological findings in patients with a novel DNM2 mutation. Neuropathology : official journal of the Japanese Society of Neuropathology 10 28971531
2023 DNM2 levels normalization improves muscle phenotypes of a novel mouse model for moderate centronuclear myopathy. Molecular therapy. Nucleic acids 8 37547294
2022 Phenotypic Spectrum of DNM2-Related Centronuclear Myopathy. Neurology. Genetics 8 36324371
2013 Myotonia in DNM2-related centronuclear myopathy. Journal of neural transmission (Vienna, Austria : 1996) 8 24366529
2014 Clinical and Pathological Features of Korean Patients with DNM2-Related Centronuclear Myopathy. Journal of clinical neurology (Seoul, Korea) 7 24465259
2022 A dog model for centronuclear myopathy carrying the most common DNM2 mutation. Disease models & mechanisms 6 35244154
2016 DNM2 mutations in Chinese Han patients with centronuclear myopathy. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 6 26908122
2021 Imaging-based evaluation of pathogenicity by novel DNM2 variants associated with centronuclear myopathy. Human mutation 5 34837441
2020 A location, location, location mutation impairs DNM2-mediated release of nascent autophagosomes from recycling endosomes. Autophagy 5 32453967
2022 mir-204-5p Acts as a Tumor Suppressor by Targeting DNM2 in Osteosarcoma Cells. Journal of healthcare engineering 4 35186244
2017 A rare case of centronuclear myopathy with DNM2 mutation: genotype-phenotype correlation. Autopsy & case reports 4 28740838
2014 Utilizing the Dyn2 dimerization-zipper as a tool to probe NPC structure and function. Methods in cell biology 2 24857727
2025 BIN1 reduction ameliorates DNM2-related Charcot-Marie-Tooth neuropathy. Proceedings of the National Academy of Sciences of the United States of America 1 40042903
2025 NSUN2-engineered human umbilical cord mesenchymal stem cell-derived exosomes ameliorate tendon injury by promoting DNM2 expression. Regenerative therapy 1 41503520
2024 The dynamin-related protein Dyn2 is essential for both apicoplast and mitochondrial fission in Plasmodium falciparum. bioRxiv : the preprint server for biology 1 38559241
2023 Implication of Dynamin-2 (DNM2) Mutations in Adult T-cell Acute Lymphoblastic Leukemia. Asian Pacific journal of cancer prevention : APJCP 1 37116148
2021 A new mutation in DNM2 gene in a large Italian family. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 1 33459893
1997 Dynamin genes Dnm1 and Dnm2 are located on proximal mouse chromosomes 2 and 9, respectively. Genomics 1 9143510
2026 Muscle-Specific DNM2 Overexpression Improves Charcot-Marie-Tooth Disease In Vivo and Reveals a Narrow Therapeutic Window in Skeletal Muscle. International journal of molecular sciences 0 41683892
2026 DNM2 lipid binding drives centronuclear myopathy and represents a potential therapeutic target. JCI insight 0 42100875
2025 A novel DNM2 variant associated with centronuclear myopathy: a case report. Frontiers in genetics 0 40259930

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