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The twin siblings exhibit mild to moderate intellectual disability and autistic symptoms but no epileptic encephalopathy. Exome sequencing revealed a genetic variant, c.1603A>G (p.Lys535Glu), in the PH domain of dynamin 1. The twin sisters studied here share the de novo variant, c.1603A>G (p.Lys535Glu) in exon 15 of DNM1, classified as likely pathogenic.
The data show that the dynamin-amphiphysin (show AMPH Proteins) helices are rearranged to form clusters upon GTP (show AK3 Proteins) hydrolysis and membrane constriction occurs at protein-uncoated regions flanking the clusters.
Together, these observations suggest that while endophilin helps shape endocytic tubules and recruit dynamin to endocytic sites, it can also block membrane fission when present in excess (show RCC1 Proteins) by inhibiting inter-dynamin interactions.
The authors show that in fibroblasts, dynamin GTP (show AK3 Proteins) hydrolysis occurs as stochastic bursts, which are randomly distributed relatively to the peak of dynamin assembly. Thus, dynamin disassembly is not coupled to GTPase (show RACGAP1 Proteins) activity, supporting that the GTP (show AK3 Proteins) energy is primarily spent in constriction.
Dynamin isoforms differentially regulate the endocytosis and apoptotic signaling downstream of TRAIL-death receptor (TRAIL-DR) complexes in cancer cells. TRAIL stimulation activates ryanodine receptor (show RYR3 Proteins)-mediated calcium release from endoplasmic reticulum stores, leading to calcineurin-mediated dephosphorylation and activation of Dyn1 (show DNM1L Proteins), TRAIL-DR endocytosis, and increased resistance to TRAIL-induced apoptosis.
Three genes in our epilepsy cohort (COQ4 (show COQ4 Proteins), DNM1, and PURA (show PURA Proteins)), accounting for 14% (3/21) of all novel genetic etiologies identified in patients with epilepsy, were subsequently confirmed in independent publications.
Study delineates the phenotypic spectrum of DNM1 encephalopathy, an emerging disease of synaptic vesicle fission characterized by severe to profound developmental delay, infantile-onset epilepsy beginning with infantile spasms, and movement disorder. The genetic landscape of DNM1 encephalopathy is notable for the recurrent c.709C>T (p.Arg237Trp) variant and localization of mutations to specific domains of the protein.
CLCb/Dyn1 (show DNM1L Proteins)-dependent adaptive clathrin-mediated endocytosis selectively altered EGF receptor (show EGFR Proteins) trafficking.
interation of DG with laminin and dynamin is involved in the regulation of AQP4 (show AQP4 Proteins) internalization
Down-regulation of Dyn1 (show DNM1L Proteins) activity enhances extracellular Nme1 (show NME1 Proteins) in human colon tumor cell lines.
dynamin is a molecular motor (show MYO1B Proteins) which would be involved in GLUT4 (show SLC2A4 Proteins) translocation by facilitating exocytosis
reveal functional differences between Dnm1a and Dnm1b isoforms in the presence of a challenge, i.e. toxic Dnm1(Ftfl), while reinforcing its effect explicitly in this model of severe pediatric epilepsy
Dynamin may facilitate Fas (show FAS Proteins)-mediated apoptotic death in the brain, and Hsp70 (show HSP70 Proteins) may protect by preventing this trafficking.
These results suggested that dynamin 1 was susceptible to the aging process, and that a reduction in dynamin 1 may result in hippocampaldependent memory deficits by disrupting endocytosis and the release of neurotransmitters.
Tissue-specific dynamin-1 deletion at the calyx of Held decreases short-term depression through a mechanism distinct from vesicle resupply.
findings support a role for HTT (show HTT Proteins) on dynamin 1 function and ER homoeostasis. Proteolysis-induced alteration of this function may be relevant to disease.
the identification of the oligomerization cycle of dynamin is an attractive potential therapeutic target to treat chronic kidney diseases .
In the developing neurons, there is a dynamin 1-, dynamin 3- and clathrin-independent pathway of synaptic vesicle recycling mediated by bulk endocytosis.
Using an inducible knockout mouse model to generate dynamin 1- and 2-deficient primary osteoclast precursors and myoblasts, it was shown that fusion of both cell types requires dynamin.
Dynamin 1 is required for memory formation.
Equine herpesvirus type 1 pUL56-induced MHC-I endocytosis required dynamin and tyrosine kinase but was independent of clathrin and caveolin-1, the main constituents of the clathrin- and raft/caveola-mediated endocytosis pathways, respectively.
This gene encodes a member of the dynamin subfamily of GTP-binding proteins. The encoded protein possesses unique mechanochemical properties used to tubulate and sever membranes, and is involved in clathrin-mediated endocytosis and other vesicular trafficking processes. Actin and other cytoskeletal proteins act as binding partners for the encoded protein, which can also self-assemble leading to stimulation of GTPase activity. More than sixty highly conserved copies of the 3' region of this gene are found elsewhere in the genome, particularly on chromosomes Y and 15. Alternatively spliced transcript variants encoding different isoforms have been described.
, dynamin, brain
, dynamin 1