Mouse dynamin 2,DNM2 ELISA Kit
- Known as:
- Mouse dynamin 2,DNM2 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0976Mo
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Sunlog
- Gene target:
- Mouse dynamin 2 DNM2 ELISA Kit
Related genes to: Mouse dynamin 2,DNM2 ELISA Kit
- Gene:
- DNM2 NIH gene
- Name:
- dynamin 2
- Previous symbol:
- -
- Synonyms:
- DYNII, DYN2, CMTDIB, CMTDI1, DI-CMTB, CMT2M
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2019-04-23
Related products to: Mouse dynamin 2,DNM2 ELISA Kit
Related articles to: Mouse dynamin 2,DNM2 ELISA Kit
- DNM2-related centronuclear myopathy (DNM2-CNM) exhibits characteristic imaging patterns, but imaging-based staging and variant-specific severity pattern remain incompletely defined. We aimed to (1) characterize muscle involvement patterns, (2) establish imaging-based severity stages and identify muscles that best distinguish severity groups, and (3) model variant- and muscle-specific age-related score patterns, with comparison to adult-onset MTM1-related CNM. - Source: PubMed
Publication date: 2026/09/25
Uy Genevieve Gucci Grace CapispisanNoguchi SatoruHayashi ShinichiroTakahashi YujiNishino Ichizo - Autophagy involves the rapid growth of phagophores through membrane addition. This growth is triggered by vesicles containing the Atg9A protein. However, Atg9A is not incorporated into mature autophagosomes. We now demonstrate that Dynamin-2 (Dnm2) colocalizes with the BAR domain protein Endophilin-B1 (EndoB1/Bif-1/SH3GLB1) and other autophagy proteins when autophagy is induced. Our data suggest that Atg9A is retrieved from phagophores via fission, with help from Dnm2. Blocking Atg9A recycling, either by mutating Dnm2, using RNA interference, or applying chemical inhibitors, results in Atg9A remaining in autophagosomes and being degraded during autophagy. Overall, these findings provide new insights into the roles of Dnm2 in autophagy. - Source: PubMed
Publication date: 2026/09/21
Caliri AndrewRiera Alejandro MartorellKolitsida PanagiotaSaha AkashMartinez Cinta IriondoItskanov SamuelSteffen JanosKoehler Carla Mvan der Bliek Alexander M - Dominant loss-of-function mutations in cause Charcot-Marie-Tooth neuropathy characterized by sensory and motor deficits associated with myelin and/or axonal abnormalities and muscle atrophy. Increasing DNM2 activity from embryogenesis has been reported to ameliorate neuromuscular phenotypes in the Charcot-Marie-Tooth mouse; however, this model displays predominantly muscle pathology and limited nerve involvement, precluding rigorous evaluation of neuropathic mechanisms and potential therapies. Here, we performed comprehensive behavioural, electrophysiological, histological and molecular analyses to characterize the mouse, which combines systemic heterozygosity for the common K562E mutation together with Schwann cell-specific deletion of wild-type . This model faithfully reproduces key clinical and pathological features of -Charcot-Marie-Tooth, including motor deficits, reduced general force and coordination, and severe sensory and motor conduction deficits associated with axonal loss, demyelination and inflammation. Mechanistically, we delineate a coherent pathological sequence that explains the profound functional deficits. In particular, a downregulation of the transcription factor EGR2, a master regulator of myelin gene expression, and of the myelin protein MPZ correlates with demyelination. To evaluate the therapeutic potential of DNM2 supplementation, post-symptomatic intrathecal delivery of AAV9-DNM2 driven by the Schwann cell-specific MPZ promoter was performed at 4 weeks. Although DNM2 expression increased in peripheral nerves (∼1.9-fold), no significant improvements were observed across behavioural, electrophysiological, structural or molecular parameters. Together, these findings establish the mouse as a robust preclinical model, recapitulating key features of -Charcot-Marie-Tooth, and provide crucial insight into the biological and temporal constraints that must guide future therapeutic strategies for -Charcot-Marie-Tooth. - Source: PubMed
Publication date: 2026/09/01
Goret MarieArbogast ThomasLaporte Jocelyn - Sepsis involves dysregulated host responses with mitochondrial dysfunction as a key mechanism, yet its immune cell landscape and clinical utility are unclear. - Source: PubMed
Publication date: 2026/09/19
Le XinFan YoufenXu SidaLi JiliangCui ShengyongJin GuoyingHuang NengYu YaohuaXu Pei - Autosomal dominant centronuclear myopathy (ADCNM), most commonly caused by mutations in the dynamin 2 (DNM2) gene, is a rare congenital myopathy characterized by progressive muscle weakness and atrophy. Myostatin, a key negative regulator of skeletal muscle mass, has shown therapeutic potential in several models of neuromuscular diseases. We hypothesized that inhibiting myostatin could counteract muscle deconditioning in ADCNM and evaluated the therapeutic potential of both genetic and pharmacological myostatin inhibition strategies in a mouse model of ADCNM. - Source: PubMed
Anne-Cécile DurieuxDavid ArnouldMathias VelardeValentine AllibertChloé ParetQuentin DebelleyEsra KizilkilicSidney ChambonEmmanuelle GirardLouise CollinAlexandre GenselJosiane CastellsAja PasternackMaximilien BowenBaptiste MorelChristophe HourdéSchaeffer LaurentOlli RitvosMarc BitounRémi MounierDamien Freyssenet