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These observations support the notion that a major function of Myosin VI in the nerve terminal is tethering synaptic vesicles to proper sub-cellular location within the bouton
These data demonstrate that generating an organized and functional actin structure in this cell requires multiple activities coordinated by myosin VI.
The androcam structure and its binding to the myosin VI structural (Insert 2) and regulatory (IQ) light chain sites are distinct from those of calmodulin.
data indicate that myosin V and VI, but not II, play related but distinct roles in regulating microtubule (MT)-based mitochondrial movement: they oppose, rather than complement, protracted MT-based movements and perhaps facilitate organelle docking
MyoVI is required for border cell migration where it stabilizes E-cadherin and Arm.
Myosin VI is crucial for correct cell morphology and maintenance of adhesive cellular contacts within epithelial cell layers.
Myosin VI stabilizes a branched actin network in actin structures (cones) that mediate the separation of the syncytial spermatids. I
The spatial and temporal expression of Myosin VI was examined by expressing a Green Fluorescent Protein tagged Myosin VI molecule, under the control of a Myosin VI-Gal4 line.
Data suggest that Echinoid mediates the dimerization of myosin VI/Jaguar in vivo which in turn regulates the reorganization and/or contraction of actin filaments to control changes in cell shape.
Miranda protein forms an apical crescent at interphase, but is ubiquitously localized at prophase in a Myosin-II-dependent manner.
Genetic characterization of the Drosophila jaguar322 mutant reveals that complete myosin VI loss of function is not lethal.
Results suggest that myosin VI does not need to dimerize via the predicted coiled coil to stabilize actin in vivo.
Backfolding of MVI regulates its ability to bind DNA and that a putative transcription co-activator NDP52 relieves the auto-inhibition of MVI to enable DNA binding. Additionally, we show that the MVI-NDP52 complex binds RNAPII, which is critical for transcription, and that depletion of NDP52 or MVI reduces steady-state mRNA levels.
The tumorigenic effect of lncRNA SOX21-AS1 in CRC cells via targeting miR-145/MYO6, providing a novel insight for CRC carcinogenesis.
Rab33b, OATL1 and Myo6 have roles in nanoparticle trafficking in HeLa cells
miR-143 and miR-145 suppress gastric cancer cell migration and metastasis by inhibiting MYO6 expression and the epithelial-mesenchymal transition, which provides a novel mechanism and promising therapeutic target for the treatment of gastric cancer metastasis.
MYO6 facilitates Salmonella invasion.Salmonella virulence effector SopB requires MYO6 to regulate the localization of phosphoinositides and Akt activation.
Data indicate filopodia formation and MYO6 motor function at endosomes and at the plasma membrane.
we describe a novel nonsense MYO6 mutation that was responsible for the hearing loss in a Brazilian family
this is the first ILDR1 and MYO6 mutations recognized in the southwest Iran. Our data expands the spectrum of mutations in ILDR1 and MYO6 genes
MYO6 could play an essential role in the growth of OSCC cells via regulation of cell cycle progression and apoptosis.
characterisation of the human myosin VI deafness mutant (R1166X) suggests that defects in cargo binding may leave myosin VI in a primed/activated state with an increased actin-binding ability
PRAS40 was downregulated in the DU145 cells following MYO6 knockdown.
knockdown of MYO6 slightly arrested cell cycle in G0/G1 phase, but remarkably increased the proportion of the sub-G1 phase of cell with the increase of apoptotic cells in colorectal cancer
study indicates that MYO6 may play an important role in gastric cancer tumorigenesis and may serve as a potential therapeutic target in human gastric cancer.
This study identified an isoform-specific regulatory helix, named the alpha2-linker, that defines specific conformations and hence determines the target selectivity of human myosin VI.
Interaction of myosin VI and its binding partner DOCK7 plays an important role in NGF-stimulated protrusion formation in PC12 cells.
Knockdown of myosin VI significantly suppressed melanoma cell viability and proliferation.
Knockdown of MYO6 markedly reduced cell viability and colony formation, as well as suppressed cell cycle progression in breast cancer cells.
MYO6 was highly expressed in hepatocellular carcinoma.
MYO6 is crucial in maintaining cell cycle and cell growth of lung cancer cells.MYO6 is highly expressed in human lung cancer tissues.
Optineurin binding to myosin VI was also decreased in tissue lysates from sporadic amyotrophic lateral sclerosis spinal cords.
Loss of MYO6 results in an accumulation of mitophagosomes and an increase in mitochondrial mass.
both AKT phosphorylation and RAC-dependent membrane ruffling were markedly reduced by depletion of either APPL1 or MYO6. These results place MYO6 and its binding partners at a central nexus in cellular signaling linking actin dynamics at the cell surface and endosomal signaling in the cell cortex.
GIPC1 forms a domain-swapped dimer in an autoinhibited conformation that hinders binding of both PlexinD1 and myosin VI. PlexinD1 binding to GIPC1 releases the autoinhibition, promoting its interaction with myosin VI. GIPCs and myosin VI interact through two distinct interfaces and form an open-ended alternating array.
indicated that decreased MYO6 levels in ksv/ksv mutants disrupt actin networks in the apical region of hair cells, thereby maintaining the normal structure of the cuticular plates and rootlets, and additionally provided a cellular basis for stereociliary fusion in Myo6 mutants
We propose that myosin VI, by removing stereociliary elements such as CDH23 as a component of the transient lateral links (which are probably required for the integrity of the immature hair bundles), allows the hair bundle and its transduction apparatus to progress in their development, so that the mechano-electrical transducer channels acquire their physiological resting tension and Ca2+-dependent adaptation properties
a plaque accretion defect as the primary manifestation of myosin VI loss in Cx43 homeostasis, is reported.
the Turner mutation was mapped to a critical region of 11 cM on chromosome 9 that includes myosin VI.
Myo1a and Myo6 play essential roles in response to intestinal mucosal injury
Disruption in optineurin and myosin VI-mediated cellular trafficking is associated with amyotrophic lateral sclerosis.
data indicate that MVI plays an important role in myogenic cells, also during their differentiation into myotubes
We postulate that this novel interaction linking MVI with the PKA pathway could be important for targeting AKAP9-PKA complex within cells and/or providing PKA to phosphorylate MVI tail domain.
Dysfunction of myosin VI is associated with slow retinal optic neuropathy and age-related macular degeneration.
homologous pairing and myosin VI-mediated transcriptional pause release account for the rapid and efficient expression of genes induced by an external stimulus
Myosin VI mediates the movement of NHE3 to the microvillus in intestinal epithelial cells.
Report no change in cardiac myosin VI expression in mouse model of dilated cardiomyopathy.
the Trip6-GRIP1-myosin VI interaction and its regulation on F-actin network play a significant role in dendritic morphogenesis
Mutated Pou4f3 has a negative role in the promoter activity of Myo6.
homozygous Myo6(tvrm89) mice display reduced ERG a-wave and b-wave components, as well as components of the ERG attributed to RPE function, indicates that myosin 6 is necessary for the generation of proper responses of the outer retina to light.
Myo6 may play a predominant pivotal role in the mechanism underlying proliferation without affecting differentiation to progeny lineages in pluripotent P19 cells.
Suggest myo6 mutations are responsible for congenital deafness and vestibular dysfunction in ENU-generated mutant mice.
Studied the crystal structure of myosin VI, (the pretransition state (PTS)), in particular the recovery stroke of Myosin VI, which was solved at 2.2 A resolution.
Data suggest that cells direct the movement of vesicles around a cell by altering the relative number of myosin Va from Gallus gallus and myosin VI from Sus scrofa.
A myosin VI deafness mutation, D179Y, uncoupled the release of the ATP hydrolysis product, inorganic phosphate (Pi), from dependency on actin binding and destroyed the ability of single dimeric molecules to move processively on actin filaments.
model reveals that myosin VI, unlike plus-end directed myosins, does not use a pure lever arm mechanism, but instead steps with a mechanism analogous to the kinesin neck-linker uncoupling mode
The stepping dynamics of single quantum-dot-labeled myoV and myoVI motors linked to a common cargo, was studied.
These results suggest that myosin VI kinetics are tuned such that the motor maintains a consistent level of mechanical tension within the cell, a property potentially shared by other mechanosensitive proteins.
a mechanism is proposed of myosin VI stepping that predicts a regulation through load of the motor's roles as transporter and anchor
2.4-A structure of a truncated version of the reverse-direction myosin motor, myosin VI, that contains the motor domain and binding sites for two calmodulin molecules
Data demonstrate that full-length myosin VI is capable of forming stable, processive dimers when monomers are clustered, which move up to 1-2 mum in approximately 30 nm, hand-over-hand steps.
unique insert is required for directionality reversal, ruling out a large class of models in which the converter domain moves toward the (-) end
further adaptations within the motor increase the magnitude and variability of the plus-end directed converter movements, and unexpectedly provide the source of the highly variable myosin VI step size
Results suggest that myosin VI and vinculin form a molecular apparatus that generates cohesive cell-cell contacts in cultured mammalian epithelia.
the crystal structure of a fragment of the myosin VI motor in the structural state represents the starting point for movement on actin; the pre-powerstroke state.
Novel features of myosin VI may be important in maintaining the converter conformation during detachment from actin. Other features may promote rapid rearrangement in structure following actin detachment that enable hydrolysis of adenosine triphosphate.
These data indicate that the myosin VI immunoanalog has an important role in pinocytosis and phagocytosis in Amoeba proteus (Pal.).
propose that for the two heads of myosin VI to coordinate their processive movement, the lever arm of the lead head must be uncoupled from the converter until the rear head detaches.
MVI, but not myosins IB or IIB, was detected in chromaffin granules isolated from bovine medulla and found to be tightly associated with the granule apical surface.
This gene encodes a protein involved intracellular vesicle and organelle transport, especially in the hair cell of the inner ear. Mutations in this gene have been found in patients with non-syndromic autosomal dominant and recessive hearing loss.
, 95F unconventional myosin
, myosin 95F
, myosin VI
, myosin heavy chain
, myosin heavy chain at 95F
, unconventional myosin VI
, unconventional myosin-6
, unconventional myosin-VI
, Snell's waltzer
, unconventional myosin