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DNM3 may be involved in risk of obsessive-compulsive disorder.
Microdeletion of DNM3 harboring miR199 and miR214 is associated with skeletal abnormalities.
DNM3 attenuates the proliferation and induces apoptosis of gastric cancer cells.
Data show that the classical dynamin DNM1 (show DNM1 ELISA Kits) and DNM3 genes reach their maximum expression levels (100% of maximal expression) in all normal central nervous system tissues studied.
Data indicate that dynamin 3 (DNM3) harbors MEIS1 (show MEIS1 ELISA Kits) binding sites and is associated with differences in mean platelet volume (MPV).
DNM3 not only participates in megakaryocyte progenitor amplification, but is also involved in cytoplasmic enlargement and the formation of the demarcation membrane system.
Dynamin (show DNM1 ELISA Kits) GTPase (show RACGAP1 ELISA Kits) regulation is altered by PH domain mutations found in centronuclear myopathy patients.
dynamin-3 and the postsynaptic adaptor Homer (show HOMER1 ELISA Kits) positions the endocytic zones near the postsynaptic density
Upon comparison of PBMC and skin samples of Sezary syndrome versus mycosis fungoides, CDO1 (show CDO1 ELISA Kits) and DNM3 were found upregulated only in Sezary syndrome.
Dynamin 3 participates in the growth and development of megakaryocytes.
In the developing neurons, there is a dynamin 1-, dynamin 3- and clathrin-independent pathway of synaptic vesicle recycling mediated by bulk endocytosis.
As low-level expression of the dynamin 3 gene in these cells could not be excluded, we have now engineered dynamin 1 (show DNM1 ELISA Kits), 2 and 3 triple KO (TKO (show MRPS12 ELISA Kits)) fibroblasts.
Data indicate that coxsackievirus and adenovirus receptor (show CXADR ELISA Kits) (CAR) internalization was lipid microdomain-, actin-, and dynamin (show DNM1 ELISA Kits)-dependent, and subsequently followed by CAR degradation in lysosomes.
Data indicate that dynamin (show DNM1 ELISA Kits), clathrin, adaptor protein complex-2 (AP2 (show TFAP2A ELISA Kits)), and amphiphysin (show AMPH ELISA Kits) contribute to the depolarization-evoked entry in endocytosis.
These findings reveal a mechanism aimed at preventing synaptic transmission failure due to vesicle depletion when recycling vesicle traffic is backed up by a defect in dynamin (show DNM1 ELISA Kits)-dependent endocytosis.
Lack of dynamin 3 does not produce an overt phenotype in mice; however, it worsens the dynamin 1 (show DNM1 ELISA Kits) KO phenotype, leading to perinatal lethality and a more severe defect in activity-dependent synaptic vesicle endocytosis.
Members of the dynamin family, such as DNM3, possess mechanochemical properties involved in actin-membrane processes, predominantly in membrane budding (Orth and McNiven, 2003
, dynamin family member
, dynamin, testicular
, Dyna III
, Dynamin III
, testicular dynamin