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The protein encoded by DNM1L is a member of the dynamin superfamily of GTPases. Additionally we are shipping Dynamin 1-Like Antibodies (126) and Dynamin 1-Like Proteins (7) and many more products for this protein.
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The authors conclude that clathrin-independent compensatory endocytosis in umbrella cells is integrin regulated and occurs by a RhoA (show RHOA ELISA Kits)- and dynamin (show DNM1 ELISA Kits)-dependent pathway.
This report describes a patient with a DNM1L mutation and abnormalities in mitochondrial fission and function. The pathogenicity and the dominant nature of the novel p.G362S mutation are demonstrated by overexpression of the mutant gene.
In contrast to the initial report of neonatal lethality resulting from DNM1L mutation and DRP1 (show CRMP1 ELISA Kits) dysfunction, our results show that milder DRP1 (show CRMP1 ELISA Kits) impairment is compatible with normal early development and subsequently results in a distinct set of neurological findings. In addition, we identify a common pathogenic mechanism whereby DNM1L mutations impair mitochondrial fission.
These findings provide new insights into MCL-1 (show MCL1 ELISA Kits) ligands, and the interplay between DRP-1 (show CRMP1 ELISA Kits) and the anti-apoptotic BCL-2 (show BCL2 ELISA Kits) family members in the regulation of apoptosis
High drp1 (show CRMP1 ELISA Kits) expression is associated with cisplatin-induced apoptosis of renal tubular epithelial cells.
This study demonstrated that Mutations in DNM1L, as in OPA1 (show OPA1 ELISA Kits), result indominant optic atrophy despite opposite effectson mitochondrial fusion and fission.
Reinitiation complexes involving initiation factors eIF2D (show EIF2D ELISA Kits), MCT-1 (show CMA1 ELISA Kits), and DENR (show DENR ELISA Kits) controls the translation of a large fraction of mammalian cellular mRNAs.
Modulation of mitochondrial fission by increased levels of pDrp1 S616.
This is the first study to identify an association between SIRT4 expression and decreased mitochondrial fission, which was driven by Drp1. SIRT4 inhibited Drp1 phosphorylation and weakened Drp1 recruitment to the mitochondrial membrane via an interaction with Fis-1.
the mitochondrial morphology of T-cell acute lymphoblastic leukemia cells were altered from elongation to fragmentation because of the extracellular signal-regulated kinase activation-mediated phosphorylation of the pro-fission factor, dynamin-related protein 1 (Drp1), at residue S616.
DNM1L was found to be involved in the regulation of collagen secretion and cardiovascular calcification.
Pharmacological inhibition of Drp1 (show CRMP1 ELISA Kits) prevents mitochondrial fission and reduces myocardial ischemia-reperfusion injury in diabetic mice.
Report a novel non-canonical function of the fission protein, DRP1 (show CRMP1 ELISA Kits) in maintaining or positively stimulating mitochondrial respiration, bioenergetics and ROS (show ROS1 ELISA Kits) signalling in adult cardiomyocyte, which is likely independent of morphological changes.
Deletion of Sirt5 (show SIRT5 ELISA Kits) in starved mouse embryonic fibroblasts increased levels of mitochondrial dynamics leading to mitochondrial accumulation of the pro-fission Drp1 (show CRMP1 ELISA Kits) and to mitochondrial fragmentation.
Podocyte apoptosis induced by hyperglycemia can be reversed by polydatin through suppressing Drp1 (show CRMP1 ELISA Kits) expression.
Heat acclimation and heat shock cause changes in mitochondrial morphology of muscle cells by acting on Drp1 (show CRMP1 ELISA Kits), which results in favoring mitochondrial fusion and fission, respectively.
findings provide new insights into the role of the Drp1 (show CRMP1 ELISA Kits)-dependent mitochondrial pathway in the osteogenic dysfunction during inflammation, indicating that this pathway may be a target for the development of new therapeutic approaches for the prevention and treatment of inflammation-induced bone destruction
Drp1 (show CRMP1 ELISA Kits) binds a mitochondrial enzyme that produces phosphatidic acid, MitoPLD (show PLD6 ELISA Kits), and regulates mitochondrial division.
Loss of Rip3 (show MPRIP ELISA Kits) significantly delays the degeneration of Drp1 (show CRMP1 ELISA Kits)-KO Purkinje neurons. Rip3 (show MPRIP ELISA Kits) loss also helps Drp1 (show CRMP1 ELISA Kits)-KO Purkinje cells maintain the elongated morphology of the mitochondrial tubules.
Drp1 (show CRMP1 ELISA Kits) does not control insulin (show INS ELISA Kits) secretion via its effect on proton leak but instead via modulation of glucose-fueled respiration.
These results suggest that neuropathology and combined cognitive decline can be attributed to hyperactivation of Drp1 (show CRMP1 ELISA Kits) in the pathogenesis of AD. Therefore, inhibitors of excessive mitochondrial fission, such as Drp1 (show CRMP1 ELISA Kits) inhibitors, may be a new strategy for AD.
The protein encoded by this gene is a member of the dynamin superfamily of GTPases. Members of the dynamin-related subfamily, including the S. cerevisiae proteins Dnm1 and Vps1, contain the N-terminal tripartite GTPase domain but do not have the pleckstrin homology or proline-rich domains. This protein establishes mitochondrial morphology through a role in distributing mitochondrial tubules throughout the cytoplasm. The gene has 3 alternatively spliced transcripts encoding different isoforms. These transcripts are alternatively polyadenylated.
, dynamin-1-like protein
, Dynamin-1-like protein
, dynamin-1-like protein-like
, dynamin related protein 1
, dynamin-like protein
, smooth muscle cell associated protein-3
, smooth muscle cell-associated protein 3
, Dnm1p/Vps1p-like protein
, dynamin family member proline-rich carboxyl-terminal domain less
, dynamin-like protein 4
, dynamin-like protein IV
, dynamin-related protein 1
, C-terminal region
, N-terminal region
, dynamin-like protein 1