ライフサイエンスコーパス: motor

1 nsitive to the nucleotide-bound state of the motor.

2 anical substrate translocation into the AAA+ motor.

3 by tethering cargo proteins to the myosin VI motor.

4 c-104 (a kinesin-3) is a key anterograde DCV motor.

5 TTLL-11 is transported by ciliary motors.

6 thering HSV particles to kinesin microtubule motors.

7 Like every motor action, these eye movements are subject to noise a

8 contractions.SIGNIFICANCE STATEMENT Accurate motor actions are made possible by continuous communicat

9 e evaluation to gradually select appropriate motor actions.

10 decisions where choices are associated with motor actions.

11 s show a selective modulation of preparatory motor activity following PA in healthy participants but

12 ical change and having objective (observable motor activity) and related subjective (energy) levels.

13 thway synapses and D1-mediated activation of motor activity.

14 In adult mice, FLARE also gave light- and motor-activity-dependent transcription in the cortex.

15 ovel videos depicting grasps or other manual motor acts.

16 tive lead-in variability reduced the rate of motor adaptation, whereas changes in visual lead-in vari

17 e somatotopy specific and how they relate to motor adaptation.

18 may reflect aspects of cerebellum-dependent motor adaptation.

19 perturbation that is essential for forelimb motor adaptation.

20 Correspondingly, vocal motor and cerebellar activity is greater during active e

21 metrics accounted for extra variance in both motor and cognitive performances, with cerebellar lesion

22 the regulation of emotions and in procedural motor and emotional memory consolidation.

23 eview the role of SERT in the development of motor and nonmotor complications in patients with PD, an

24 Here we examined how the abundance of motor and nonmotor cross-linkers affects the speed of cy

25 diction as a unifying cerebellar function in motor and nonmotor domains.

26 nophilin adaptor protein over its associated motor and offer an unexpected mechanism by which filamen

27 regeneration and reinnervation of muscle by motor and sensory afferents is completed in the peripher

28 neurofilament was performed to differentiate motor and sensory axons on nerve cross sections.

29 We measured 6920 synapses in mouse motor and sensory cortices using three-dimensional elect

30 Whether gastrointestinal motor and sensory function is primary cause or secondary

31 s such an approach and consists of rerouting motor and sensory nerves from the residual limb towards

32 rodegenerative diseases including hereditary motor and sensory neuropathy with proximal dominant invo

33 eal that CPH1 functions as a hub linking key motor and structural proteins that contain intrinsically

34 d by altering the number of active molecular motors and clutches.

35 egulate the formation of networks with Myo7a motors and coordinate force sensing in stereocilia.

36 h a significantly slower rate of functional, motor, and cognitive deterioration (all p < 0.001), inde

37 essful ageing was defined as good cognitive, motor, and respiratory functioning, along with absence o

38 luding disability status, visual, cognitive, motor, and sensory testing, as well as qualitative and q

39 such as photoresponsive materials, molecular motors, and photoactivated drugs.

40 o all other groups in the occipital, sensory-motor, anterior cingulate and supplementary motor cortic

41 ry and emotional regulation, and the ACC has motor areas and is thought to be important for error det

42 may interact with the portal protein during motor assembly, as predicted for several bacteriophages.

43 ng a model combining information on age, non-motor assessments, DAT imaging, and CSF biomarkers.

44 luid, composed of microtubules and molecular motors, autonomously flows through meter-long three-dime

45 of the spinal cord and myelinate peripheral motor axons, we assayed perineurial glial development, m

46 tochondrial metabolism and further affecting motor behavior in HD mice, thus constituting a promising

47 ating sensory responsiveness and controlling motor behavior.

48 ve dye optical imaging and somatosensory and motor behavioral tests to characterize the consequences

49 ic reward system and can reduce drug-induced motor behaviors, craving and dependence.

50 HMM) using quartz crystal microbalance; and motor bioactivity with ATPase assay, on a set of model s

51 isms to selectively affect EEG signatures of motor but not attentional processes.

52 isomycin (ANI) into anatomically reorganized motor, but not posterior parietal, cortex eliminated beh

53 head (TH) that contributes in propelling the motor by 16 nm have not been quantified.

54 the posterior putamen and other areas of the motor circuit during tapping in TD patients, but not in

55 an altered pattern of activation within the motor circuitry.

56 Longitudinal motor, cognitive, and imaging scores were correlated wit

57 ating that predicted sensory consequences of motor commands cancel sensory signals.

58 f our arm, changing the relationship between motor commands that our brain sends to our arm muscles a

59 els that use (efferent) information from our motor commands to predict and attenuate the sensory cons

60 rain needs to predict how the body reacts to motor commands, but how a network of spiking neurons can

61 avy chain of cytoplasmic dynein-1, a 1.4-MDa motor complex that traffics organelles, vesicles, and ma

62 e cells are known to encode only sensory and motor context.

63 n of mammalian CS systems that improved fine motor control in higher primates.

64 for enabling enhanced and more natural fine motor control of paralyzed limbs by BCI-FES neuroprosthe

65 onnectivity mainly in areas of sensorial and motor control, a result supported by the dFNC outcome an

66 on the broader neurobiology of emotions and motor control.

67 r photo-activation, enabling light-dependent motor control.

68 aviours such as reward-related learning, and motor control.

69 osition is automatically set using a stepper motor controlled by a microcontroller.

70 Lesioned mice showed normal motor coordination, balance, and general locomotion.

71 mpaired muscle grip strength, and defects in motor coordination.

72 tion (TMS) over the hand area of the primary motor cortex (M1) when humans tracked with the eyes a vi

73 In our case, the target was the primary motor cortex (M1).

74 connections between separate neural sites in motor cortex (MC).

75 These results suggest that motor cortex acquires skillful control by leveraging bot

76 psilateral activity suppresses contralateral motor cortex and, accordingly, that inhibiting ipsilater

77 has been made using rodents to establish the motor cortex as an adaptive structure that supports moto

78 y 30 min over the hand representation of the motor cortex at an interstimulus interval mimicking the

79 Changes in neural activity occur in the motor cortex before movement, but the nature and purpose

80 l current stimulation of the rat (all males) motor cortex consisting of a continuous subthreshold sin

81 ulation therapies in addition to the primary motor cortex for patients who do not respond adequately

82 by previous noninvasive TMS studies of human motor cortex indicating a reduction of corticospinal exc

83 This manifold-based view of motor cortex may lead to a better understanding of how t

84 immediately after lesions in the adult mouse motor cortex restored damaged cortical pathways.

85 We recorded myogenic MEPs after transcranial motor cortex stimulation in 6 lambs aged 1-2 days.

86 diated by synaptic plasticity in a region of motor cortex that, before lesions, is not essential for

87 dapting internal model of visuomotor gain in motor cortex while two macaques performed a reaching tas

88 vo tractography, in addition to the cerebral motor cortex, major portions of CPC streamlines leave th

89 EEG was recorded over leg and hand area of motor cortex.

90 and physiological inhibition in the primary motor cortex.

91 Here, we investigated how motor cortical activity changed in the presence of an ob

92 Motor cortical fibrin(ogen) deposition was significantly

93 n the spike-field coherence of a rat primary motor cortical neuron to the LFP theta rhythm.

94 We previously reported that embryonic motor cortical neurons transplanted immediately after le

95 lent joint-angles (intrinsic coordinates) in motor cortices.

96 -motor, anterior cingulate and supplementary motor cortices.

97 I, which structurally connects the bilateral motor cortices.

98 but rather a single movement that optimizes motor costs.

99 The motor defects were worsened by mecamylamine, a selective

100 /2b neurons, also rescued the locomotion and motor defects, but not the defects in neuromuscular junc

101 mpaired brain development and behavioral and motor defects.

102 y was compromised during the early stages of motor deficit development.

103 ral-dopaminergic neuronal system exacerbates motor deficit.

104 ggravates the ischemia-induced brain damage, motor deficits and mortality.

105 nd is associated with impaired cognitive and motor development and increased morbidity and mortality.

106 processing speed, auditory memory, and fine motor dexterity.

107 ired about 4 times fewer participants than a motor diagnosis alone.

108 For required sample size, PFS with a motor diagnosis or total motor score progression require

109 utation carriers who have not yet received a motor diagnosis.

110 ilar findings were obtained by adjusting for motor disability (P < .05, permutation-corrected P = .06

111 formed our understanding of pediatric ocular motor disease at the prenuclear and infranuclear levels.

112 alling could play a major role in initiating motor disease.

113 conserved regulator of dynein, binds to its motor domain and induces a tight microtubule-binding sta

114 First, the motor domain attains the poststroke conformation without

115 sights into structural changes in the myosin motor domain that are triggered upon F-actin binding and

116 er arm rotation is mostly uncoupled from the motor domain.

117 ucture indicates how tension between the two motor domains keeps their cycles out of phase in order t

118 ining thin filaments that allows the head or motor domains of myosin from the thick filaments to bind

119 The AAA+ motor-driven acceleration of Rpn11 is therefore importan

120 Myo2p, not Myp2p, is likely to be the major motor driving actomyosin ring contractility.

121 to measure the axial movement of the myosin motors during the diastole-systole cycle under sarcomere

122 2 in the writhing assay and without inducing motor dysfunction after sc administration in mice.

123 orated multiple RTT-like features, including motor dysfunction and breathing irregularities, in both

124 iptomic dysregulation even after substantial motor dysfunction and pathology were observed.

125 treatment) remains unknown, although spastic motor dysfunction has been related to the hyperexcitabil

126 ter injury is often accompanied by orofacial motor dysfunction, but little is known about the structu

127 bute to behavioral deficits in AS, including motor dysfunction.

128 r that results in debilitating cognitive and motor dysfunction.

129 ture, reduced ATP production, and flight and motor dysfunction.

130 Motor dysfunctions were chiefly associated with the ante

131 t this choice effect can be dissociated from motor effects on saccade initiation and execution.SIGNIF

132 r disorder (RBD) is characterised by complex motor enactment of dreams and is a potential prodromal m

133 ere the sensory-evoked signal suppresses the motor-encoding signal to transform the spatial informati

134 ith the exception that it was not subject to motor (execution) noise.

135 early development of combined autonomic and motor features but not MSA phenotype (multivariate HR 1.

136 the two pathways' contribution to different motor features using SPN type-specific chemogenetic stim

137 ers that control the forces generated within motor-filament arrays and provide insight into the self-

138 Understanding the physics of such motor-filament materials is critical to developing a phy

139 ime in levodopa-treated patients with PD and motor fluctuations, and this effect is maintained for at

140 d model, setting the stage for more advanced motors for functional dynamic systems.

141 ease (PD) patients experience loss of normal motor function (hypokinesia), but can develop uncontroll

142 faster and more complete recovery of forepaw motor function (P < 0.05).

143 onths with progression, correlations between motor function and biomarkers, and hazard ratios analyze

144 n rural Bangladesh we examined cognitive and motor function and scholastic achievement in a cohort of

145 teral parietal cortices also correlated with motor function improvement, consistent with the increase

146 key factor in the detrimental outcome of the motor function in amyotrophic lateral sclerosis.

147 ersive learning as well as markedly affected motor function including disordered coordination.

148 ion, a R502P amino acid substitution, on the motor function is unclear.

149 Infant motor function scales (Test of Infant Motor Performance

150 Motor function scores (MFS) and compound muscle action p

151 Motor function was altered, and specific effects were fo

152 cted effect of ageing on episodic memory and motor function with advanced stages of HIV infection sug

153 e peripheral nervous system is essential for motor function, and uncontrolled SC proliferation occurs

154 is correlated with improved neurological and motor function, as well as with preservation of neuronal

155 bserved during RBD episodes exhibit improved motor function, relative to baseline states during wake

156 sed on a well-supported theory of cerebellar motor function, which ascribes to the cerebellum a role

157 STN transmission and patterning and improved motor function.

158 lamic development, and thereby cognitive and motor function.

159 f cerebellar Purkinje cells and a decline in motor function.

160 mulation (DBS) within circuits that modulate motor function.

161 This loss greatly affects full recovery of motor function.

162 opment and degeneration in adulthood impairs motor function.

163 hortly after exposure (30 min), and impaired motor functions (falls: +83%; time top: -43%; time botto

164 -generated PA in the regulation of kinesin-1 motor functions and breast cancer metastasis and suggest

165 e overall fundamental contribution of D2R in motor functions and explains some of the side effects el

166 exocytosis in MB neurons and alters specific motor functions of 1-year-old male mice.

167 While the packaging motors have been described in some detail, the maturatio

168 Brain-computer interface-assisted motor imagery (MI-BCI) or transcranial direct current st

169 mean on the Wide Range Achievement Test-4), motor impairment (defined as a percentile rank of </=5 o

170 on was independent of measures of anxiety or motor impairment and could be overcome by strong motivat

171 e muscle hyperexcitability and contribute to motor impersistence.SIGNIFICANCE STATEMENT Recent eviden

172 agonists in reducing psychostimulant-induced motor impulsivity.

173 quently caused by non-assembly of dynein arm motors into cilia and flagella axonemes.

174 cerebellar Purkinje cells for the control of motor learning and timing.

175 s able to predict participant performance in motor learning by using parameters estimated from the de

176 Previous studies have shown that motor learning results in at least two important neuroph

177 we studied performance during an explorative motor learning task and a decision-making task which had

178 ortex as an adaptive structure that supports motor learning.

179 t inhibiting ipsilateral regions can improve motor learning.

180 nce can be exerted directly upon the primary motor (M1) and somatosensory (S1) cortical areas via the

181 Dorsal premotor (PMd) and primary motor (M1) cortices play a central role in mapping sensa

182 ression and anxiety frequently accompany the motor manifestations of isolated adult-onset focal dysto

183 Disrupting synapses and motor maps by infusions of anisomycin (ANI) into anatomi

184 ability in learning and in the generation of motor memories could be predicted from baseline resting-

185 We studied the modularity in long-term motor memories in the context of locomotor adaptation us

186 follow-through movements affects the rate of motor memory formation.

187 from this vulnerable state by strengthening motor-microtubule electrostatic interactions also increa

188 nersen group than in the control group had a motor-milestone response (37 of 73 infants [51%] vs. 0 o

189 In Saccharomyces cerevisiae, the myosin V motor Myo2 binds the vacuole-specific adapter Vac17 to a

190 nanticipated structural requirement that TFP motors need to have a minimal amount of effective angula

191 SCPs migrate along the visceral motor nerve to the vicinity of the forming adrenal gland

192 ATP is also released from sensory-motor nerves during antidromic reflex activity, to produ

193 animals execute precise actions using sparse motor networks, we imaged the activity of a complete ens

194 internal model before movement could improve motor neural prostheses being developed for people with

195 scular junction (NMJ) dysfunction and spinal motor neuron (MN) loss.

196 hy (SMA) is caused by diminished Survival of Motor Neuron (SMN) protein, leading to neuromuscular jun

197 iency of the ubiquitously expressed Survival Motor Neuron (SMN) protein.

198 o showed that TBPH mutants displayed reduced motor neuron bursting and coordination during crawling a

199 ion of RNA:DNA hybrid structures, leading to motor neuron death.

200 how that Zfp106 knockout mice develop severe motor neuron degeneration, which can be suppressed by tr

201 electrical activity to decode accurate alpha-motor neuron discharges across five lumbosacral segments

202 l sclerosis (ALS) is a multifactorial lethal motor neuron disease with no known treatment.

203 ons that have been associated with increased motor neuron excitability and decreased inhibition.

204 sing ADL neurons and their post-synaptic SMB motor neuron partners via increased expression of the od

205 iatric changes, movement disorders and upper motor neuron signs.

206 cending neurons, which drive the jump muscle motor neuron to trigger an escape take off.

207 ts (the muscle fibers innervated by a single motor neuron) and manipulating patterns of activation of

208 preservation of myelinated white matter and motor neurons and an increase in axonal reinnervation of

209 f polyglutamine-expanded AR causes damage to motor neurons and skeletal muscle cells.

210 NCE STATEMENT The inadequate excitability of motor neurons and their output, the neuromuscular juncti

211 ified a defect in repetitive firing of lower motor neurons as a novel contributor to intensive care u

212 Reticulospinal neurons project to spinal motor neurons controlling hand muscles and extensively s

213 e the human disease-with progressive loss of motor neurons in heterozygous animals.

214 ubcortical levels, in particular sensory and motor neurons in the brainstem and thalamus.

215 eroxide dismutase (SOD1) selectively affects motor neurons in the central nervous system (CNS), causi

216 When activating muscles, motor neurons in the spinal cord also activate Renshaw c

217 that aberrant splicing of genes expressed in motor neurons is involved in SMA pathogenesis, but incre

218 Repletion of this isoform of Agrin in the motor neurons of SMA model mice increases muscle fiber s

219 d in trans within satellite cells and within motor neurons via the neuromuscular junction.

220 cular atrophy (SMA) is caused by the loss of motor neurons, but astrocyte dysfunction also contribute

221 ial mCherry did not transfer to G85R SOD1YFP motor neurons, suggesting that neither RNA nor organelle

222 y precedes dendritic arborization of primary motor neurons, suggesting that the structured neuropil c

223 receptor 1 (EphB1) is upregulated in injured motor neurons, which in turn can activate astrocytes thr

224 neurodegeneration of the corticospinal tract motor neurons.

225 provide recurrent inhibitory feedback to the motor neurons.

226 crease in axonal reinnervation of the lumbar motor neurons.

227 sgenic restoration of Zfp106 specifically in motor neurons.

228 harcot-Marie-Tooth type-2, distal hereditary motor neuropathies, spinal muscular atrophy with parkins

229 Distal hereditary motor neuropathy is a heterogeneous group of inherited n

230 es have been implicated in distal hereditary motor neuropathy, the genetic causes remain elusive in m

231 om the decision-making task and the separate motor noise measurement.

232 hat the emergence of mature topography among motor nuclei involves a novel interplay between spontane

233 es in serotonergic innervation preceding the motor onset of Parkinson's disease.

234 ue, or whether distraction was tested during motor or nonmotor cognitive tasks.

235 Motor output also always includes a non-linear remnant r

236 Importantly, hand motor output and hand dexterity increased in individuals

237 temporal characteristics of the feedforward motor output during the decay of learning.

238 scaling sustains strength of the respiratory motor output following months of inactivity, thereby sup

239 tive response whereby feedforward changes in motor output mirror both the amplitude and temporal stru

240 ple cell types, potentially influencing both motor output pathways and nucleo-olivary feedback.

241 encode information about sensory signals and motor outputs.

242 possible for persons suffering from complete motor paralysis but intact cognitive and emotional proce

243 eticulospinal tract is one of the descending motor pathways involved in recovery of hand function aft

244 g aiming to detect presymptomatic changes in motor patterning.

245 This S1 photoinhibition did not impair basic motor patterns, post-perturbation completion of the acti

246 and postural instability and gait difficulty motor PD subtype in linear regression analysis, but stag

247 sfunction and degeneration as assessed using motor performance and retinal degeneration assays respec

248 basal ganglia neurodevelopment and declined motor performance in high Mn exposed children.

249 Infant motor function scales (Test of Infant Motor Performance Screening Items [TIMPSI], The Children

250 as showed significant correlations with fine motor performance, indicating a possible link between al

251 Before a motor phenotype, animal models of HD show aberrant corti

252 human PD symptoms as they only exhibit mild motor phenotypes, minor dopamine metabolism abnormalitie

253 viously demonstrated that spinal respiratory motor plasticity elicited by acute intermittent hypoxia

254 Evoking motor potentials are an objective assessment method for

255 the contribution of fundamental sensory and motor processing at subcortical levels to FXS pathology.

256 We measured the density of the adsorbed motor protein (heavy meromyosin, HMM) using quartz cryst

257 and spindle positioning, are mediated by the motor protein cytoplasmic dynein, which produces force o

258 a yeast two-hybrid screen, we identified the motor protein Kif15 as a potential interacting partner o

259 While interactions with and functions for MT motor proteins are well characterized and extensively re

260 the structures and chemomechanical cycles of motor proteins have been extensively investigated, the s

261 are controlled by nonmuscle myosin II (NMII) motor proteins, which are tightly regulated via the phos

262 located with cerebellar areas implicated for motor (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) i

263 fferent, perhaps somewhat opposite, roles in motor recovery after brain injury.SIGNIFICANCE STATEMENT

264 One metastate is associated with sensory and motor regions, and the other involves areas related to h

265 ly described cingular-prefrontal emotion and motor regulation network.

266 tress and inhibition of non-muscle myosin II motors, respectively.

267 laxed execution, was associated with speeded motor responses without an accuracy trade-off, and an am

268 Sensory and motor RSNs showed greater cohesion and metastability, li

269 These results imply that the motor's gait follows a rotary hand-over-hand mechanism.

270 tensively investigated, the sensitivity of a motor's velocity in response to a force is not well-unde

271 liably associated with clinical improvement (motor score of the Unified Parkinson Disease Rating Scal

272 le size, PFS with a motor diagnosis or total motor score progression required about 4 times fewer par

273 Neuromuscular Disorders, and Alberta Infant Motor Score) and putative physiological and molecular bi

274 r disorder, but not cognitive dysfunction or motor severity.

275 indings indicated that in addition to output motor signals, vM1 also sends preparatory signals to vS1

276 hat the oculomotor system has access to hand motor signals.

277 Sleep spindles promote the consolidation of motor skill memory in young adults.

278 pproach, social interactions, and repetitive motor stereotypies that are relevant to ASD.

279 ebellum, although traditionally considered a motor structure, has been increasingly recognized to pla

280 tein binding and single cell-based flagellar motor switching analyses.

281 They have been associated with multiple non-motor symptoms in PD and have important clinical consequ

282 The motor symptoms of Parkinson's disease (PD) are linked to

283 o better understand its interaction with the motor symptoms of the disease.

284 We assessed the interval from onset of motor symptoms to onset of dementia, and overall surviva

285 y shaped by predictive mechanisms run by the motor system and based on the integration of feedforward

286 the actual mechanistic contributions of the motor system to sensory processing are unknown.

287 isorder falls short of the properties of the motor system.

288 d an interface between the basal ganglia and motor systems, and its ability to regulate arousal state

289 r reaction times during a startle cue in all motor tasks.

290 e mammalian kinesin-4 KIF21B is a processive motor that can accumulate at microtubule plus ends and i

291 n VIIa is a slow, high-duty ratio, monomeric motor, this altered hydrolysis rate would reduce activit

292 omatin remodelers use a helicase-like ATPase motor to reposition and reorganize nucleosomes along gen

293 e response of individual bacterial flagellar motors under stepwise changes in external osmolarity.

294 A motor unit (MU) coherence analysis was used to capture t

295 By examining the activity of individual motor units (the muscle fibers innervated by a single mo

296 tead, many of these components have multiple motor units within the optic lobe and are organized in a

297 Humans exhibit considerable motor variability even across trivial reaching movements

298 centers is derived from both industrial and motor vehicle emissions.

299 ation, a new class of light-driven molecular motors was designed, synthesized, and studied.

300 stepping behavior of kinesin-1 and -2 family motors with different length neck-linker domains.