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Members of the dynamin family, such as DNM3, possess mechanochemical properties involved in actin-membrane processes, predominantly in membrane budding (Orth and McNiven, 2003 [PubMed 12517701]).[supplied by OMIM, Mar 2008].. Additionally we are shipping Dynamin 3 Antibodies (61) and Dynamin 3 Kits (2) and many more products for this protein.
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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 Proteins) 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 Proteins) 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 Proteins) GTPase (show RACGAP1 Proteins) regulation is altered by PH domain mutations found in centronuclear myopathy patients.
dynamin-3 and the postsynaptic adaptor Homer (show HOMER1 Proteins) positions the endocytic zones near the postsynaptic density
Upon comparison of PBMC and skin samples of Sezary syndrome versus mycosis fungoides, CDO1 (show CDO1 Proteins) 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 Proteins), 2 and 3 triple KO (TKO (show MRPS12 Proteins)) fibroblasts.
Data indicate that coxsackievirus and adenovirus receptor (show CXADR Proteins) (CAR) internalization was lipid microdomain-, actin-, and dynamin (show DNM1 Proteins)-dependent, and subsequently followed by CAR degradation in lysosomes.
Data indicate that dynamin (show DNM1 Proteins), clathrin, adaptor protein complex-2 (AP2 (show TFAP2A Proteins)), and amphiphysin (show AMPH Proteins) 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 Proteins)-dependent endocytosis.
Lack of dynamin 3 does not produce an overt phenotype in mice; however, it worsens the dynamin 1 (show DNM1 Proteins) 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
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