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1 t the mechanisms that make these MEK mutants hyperactive.
2 runcation of this domain renders the channel hyperactive.
3 sting GluN2B-containing NMDARs in the KO are hyperactive.
4 d L residues and found that the majority are hyperactive.
5 NE1s, prompted these retroelements to become hyperactive.
6 jections, could move effectively and even be hyperactive 72 h after the last L-DOPA injection when do
8 these results point to a detrimental role of hyperactive ADAM10 at the HD synapse and provide preclin
13 ed that in PTEN-mutated endometrial cancers, hyperactive Akt signaling downregulates progesterone rec
17 hyperresponsiveness in PTSD may arise from a hyperactive alerting/orienting system in which processes
19 dylinositol-3-phosphate (PI3P) by generating hyperactive alleles of the yeast phosphatidylinositol 3-
20 show that common VCP disease mutants act as hyperactive alleles with respect to regulation of Mitofu
21 ymorphism Leu33Pro (rs5918, Pl(A2)) produces hyperactive alphavbeta3 receptors that influence whole-b
24 of whom 51 (58.6%) were of mixed, 10 (11.5%) hyperactive and 26 (29.9%) hypoactive delirium subtypes.
28 t allele of Arabidopsis cry1 is biologically hyperactive and seems to mimic the ATP-bound state of cr
30 n schizophrenia, the anterior hippocampus is hyperactive and shows reduced task-related recruitment,
31 ice that lack natural IELs are metabolically hyperactive and, when fed a high-fat and high-sugar diet
33 pite being disinhibited, STN neurons are not hyperactive, and (4) STN activity opposes striatopallida
35 that the common high risk Arg-325 variant is hyperactive, and thus may be targeted for inhibition to
36 ggregates in the cell membrane, while insect hyperactive antifreeze proteins (AFP) are soluble and ge
37 restingly, CRPC tumors continue to depend on hyperactive AR signaling and will respond to potent seco
38 on site on AR results in a transcriptionally hyperactive AR, suggesting that the proliferative effect
40 in diseases in which the carotid bodies are hyperactive at rest, e.g. essential hypertension, obstru
41 ctional motion, have microtubule-independent hyperactive ATPase activity, and nucleotide-independent
43 but complete removal of the brake can induce hyperactive autoubiquitination and E3 self destruction.
46 uit hyperexcitability, including anxiety and hyperactive behavior, attention deficit disorder, and se
48 iceptive dose-response (ED50) was tested and hyperactive behaviors such as jumping and scratching wer
52 1, and CDKs 1, 2, and 4) in melanomas with a hyperactive BRAF oncogene, indicating a dominant role of
53 we analyzed protein-protein interactions of hyperactive BRAF(V)(600E) and wild-type BRAF (BRAF(WT)).
56 no-associated virus selectively ablated ErbB-hyperactive cancer cells while sparing ErbB-normal cells
60 ndant inhibitory REs to achieve the level of hyperactive CARD11 signaling required to support lymphom
61 , in which 11 sites were mutated to Ala, was hyperactive, causing increased inward transport of phosp
62 or for promoting cell death of uncontrolled, hyperactive CD8(+) T cells to prevent immunopathology.
63 ory protein, which inhibits Cdk5/p35 and the hyperactive Cdk5/p25 activities in test tube experiments
64 because the accumulation of the deregulated, hyperactive Cdk5/p25 complex in human brains has been im
66 uffering from autoimmune disorders possess a hyperactive cellular phenotype where tolerance to self-a
70 ctional driver lines consistently reproduced hyperactive climbing whereas strong or weak artificial d
73 tal multi-organ autoimmunity associated with hyperactive conventional T cell responses and poor Treg-
75 Genetic depletion of TLR4 or SPAK normalizes hyperactive CSF secretion rates and reduces PHH symptoms
77 tivation state, which we call "hyperactive." Hyperactive DCs induce potent adaptive immune responses
79 r interaction between days of hypoactive and hyperactive delirium and adjusted for baseline and in-ho
80 score less than or equal to 0 and a day with hyperactive delirium as a day with positive Confusion As
85 ostatic mechanisms, (4) STN neurons were not hyperactive, despite being disinhibited, (5) optogenetic
86 t of choice in adults with attention-deficit hyperactive disorder (ADHD) and some studies were conduc
88 cells in vitro, which were attributed to the hyperactive DNMT1 or KIT, because inactivation of KIT or
89 is that developing Pten-depleted neurons are hyperactive due to increased excitatory synaptogenesis u
90 epicted by abnormal aortic arch development, hyperactive ectopic blood vessel sprouting, and aberrant
92 acid substitutions in this region produce a hyperactive enzyme complex, suggesting a role for the N-
95 glycemia in MPN mouse models correlated with hyperactive erythropoiesis and was due to a combination
97 ike or depression-like behaviors, as well as hyperactive fear circuits, glucocorticoid receptor hyper
98 Photoreceptor degeneration also triggers hyperactive firing of RGCs, obscuring light responses in
99 hyperacusis have been linked to abnormal and hyperactive firing patterns within the auditory system,
103 39 was abrogated by both the expression of a hyperactive GAC(K320A) allele and the addition of the tr
104 glucokinase-deficient bacterium, uncovers a hyperactive GCK variant with substantially reduced coope
105 ses osteoblast-specific marker expression in hyperactive Gja1(Jrt)/+ osteoblasts and may also increas
106 atement was associated with the D2R-mediated hyperactive GSK3 via Akt inhibition in the vHip and PFC.
108 n during cortical development, the transient hyperactive GSK3beta likely accounts for the cortical sp
109 We found that Nedd4-2 heterozygous mice are hyperactive, have increased basal synaptic transmission
110 tations T407A and S411A in motif V exhibit a hyperactive helicase phenotype, leading to the regulatio
111 ayed impaired gap junction communication and hyperactive hemichannels, confirmed by dye transfer, pat
116 acutely to PNS rats overrides programming of hyperactive HPA axis responses to immune challenge in a
118 enhanced DC activation state, which we call "hyperactive." Hyperactive DCs induce potent adaptive imm
120 cells demonstrated dynamic effects, by which hyperactive IL-2R signaling promoted compensatory transc
125 partially mediated the relationship between hyperactive impulsive symptoms and both poor focused att
126 r the categorical disorder of ADHD influence hyperactive-impulsive and attentional traits in the gene
127 r executive inhibition deficiency related to hyperactive-impulsive behavior in ADHD, further emphasiz
129 Active line represents a valid model for the Hyperactive-Impulsive subtype of ADHD and therefore may
130 te a pathway from polygenic risk for ADHD to hyperactive-impulsive symptoms through white matter micr
131 Regressions of childhood inattentive and hyperactive-impulsive symptoms were conducted to predict
133 estational age is related to inattentive and hyperactive/impulsive symptoms in children and adolescen
137 pk1 activity in vivo, we found that Fpk1 was hyperactive in cells lacking Gin4, a protein kinase prev
139 versive processing and is hypothesised to be hyperactive in depression, contributing to the generatio
142 her peripheral and central chemoreflexes are hyperactive in HFpEF and if chemoreflex activation exace
145 th this finding, Hippo signaling is markedly hyperactive in mammalian Dlg5(-/-) tissues and cells in
147 rtico-striatal-thalamic circuit is tonically hyperactive in mutants, but becomes hypoactive during so
148 yl arginine deiminases have been shown to be hyperactive in neurodegenerative diseases including mult
149 Thus, activity in lOFC, which is known to be hyperactive in obsessive-compulsive disorder, may be res
151 Herein, we report that Depdc5cc+ mice were hyperactive in open-field testing but did not display an
152 t, Runx2 is activated by signals known to be hyperactive in PCa including the RAS/MAP kinase pathway,
153 mstances under which the hippocampus becomes hyperactive in preclinical stages of Alzheimer's disease
154 g trend, in that CA3 cells in aged rats were hyperactive in proximal CA3, but possibly hypoactive in
156 kinson disease patients are dysregulated and hyperactive in response to stimulation with pathologic a
157 ting alpha3DeltaN proteasomes are intact but hyperactive in the hydrolysis of fluorogenic peptide sub
158 re, we show that the vHIP-mPFC projection is hyperactive in the Mecp2 knockout mouse model of the aut
159 , both Plxna4(+/-) and Plxna4(-/-) mice were hyperactive in the open field assay while Plxna4(-/-) mi
160 at contain these mutations are catalytically hyperactive in vitro and in cells, and their ectopic exp
161 on's disease, at an age when the neurons are hyperactive in vivo and the mice begin to exhibit locomo
163 nts who have NLRP3 mutations and suffer from hyperactive innate responses are defective in controllin
165 vation of its expression contributes to both hyperactive intracellular Ca(2+) oscillations and fast c
168 f endogenous PI(3,5)P(2) by the fab1(T2250A) hyperactive kinase mutant also inhibited the lipid mixin
169 or suppressor genes, whereas PKC412 inhibits hyperactive kinase signaling, which is essential for can
170 that in Cc2d1a-deficient male mice PDE4D is hyperactive, leading to a reduction in cAMP response ele
173 e therefore established an in vivo model for hyperactive mast cells by specifically ablating the NF-k
174 Our results provide in vivo evidence that hyperactive mast cells can exacerbate inflammatory disor
175 , SLC32A1) in histaminergic neurons produced hyperactive mice with an exceptional amount of sustained
178 n of eIF4E and its increased availability by hyperactive mTOR and to require phosphorylation of eIF4E
182 Importantly, increased mitotic activity and hyperactive mTOR signaling was also observed in recently
185 pocampal neurons in vitro, but the impact of hyperactive mTORC1 on axon growth in vivo and the mechan
188 th mutations of MTOR, TSC1, TSC2 or PTEN and hyperactive mTORC1 signalling are associated with better
190 gic substrate that accumulates in cells with hyperactive mTORC1, such as kidney cells with mutations
193 al therapeutic targets due to their frequent hyperactive mutations and overexpression found in cancer
194 ype previously observed in plants expressing hyperactive MYC transcription factors that cannot bind J
195 cleaved by active caspases, which released a hyperactive, N-terminal fragment that translocated to th
196 valuable for studying the in vivo effects of hyperactive Nav1.6 and the response to therapeutic inter
198 e mice displayed hypertension, hyperkalemia, hyperactive NCC, and other features fully recapitulating
200 A decline in GABAAR signalling triggers hyperactive neurological disorders such as insomnia, anx
201 ate that toxic fatty acids (FAs) produced in hyperactive neurons are transferred to astrocytic lipid
203 ough even restricted influx of Rho-deficient hyperactive neutrophils exacerbated lipopolysaccharide-m
205 rtially restored patterning, suggesting that hyperactive Nodal signalling contributes to the gastrula
209 of the CDKN2A/2B cell-cycle regulators, and hyperactive NOTCH1 signaling play prominent roles in the
210 main of M(pro) (M(pro)C) locks M(pro) into a hyperactive octameric form that is hypothesized to promo
212 albicans tetraploid cells are metabolically hyperactive on this medium with higher rates of fermenta
214 Four gain-of-function mutations that form a hyperactive or deregulated C3 convertase have been ident
224 CD300f-deficient dendritic cells displayed hyperactive phagocytosis of apoptotic cells, which stimu
225 tabolically, the DeltascmR strain displays a hyperactive phenotype relative to wild type and overprod
229 rs responsible for these failures by linking hyperactive PI3K to mis-regulation of Polo-like kinase 1
233 entiviral particles (LPs) as carriers of the hyperactive piggyBac transposase protein (hyPBase), we d
234 alysis from TCGA raised the possibility that hyperactive PPAR signaling, either due to PPAR gamma gen
244 evations in D2/3 receptor availability and a hyperactive reward processing network, underlies mania.
246 Specifically, hypoactive medial OFC and hyperactive right hippocampus responses to stress were e
250 y, we demonstrated that AID mutations caused hyperactive Set2 in vivo and displayed a synthetic inter
253 sted that reinforcing feedback is central to hyperactive signaling in a diversity of cell fate progra
254 voked Ca(2+) signals by PGE2 occurs through "hyperactive signaling junctions," wherein cAMP is locall
258 sed TORC1 activity, whereas cells containing hyperactive Snf1 display a PAS kinase-dependent decrease
259 ith marked cortical pathology, we found that hyperactive somatostatin interneurons disinhibited layer
260 eonatal bradycardia/apnea, feeding problems, hyperactive startle reflex), severe postnatal progressiv
262 ferentiated epithelial cells by expressing a hyperactive STAT5 mutant in the mammary gland during pos
264 change (hysteresis) and gradually attains a hyperactive state in which it is more active than it was
265 bilization of enzymes by ligand binding: the hyperactive state is only reached through ATP hydrolysis
266 g deconjugation of NEDD8 traps the CRLs in a hyperactive state, thereby leading to auto-ubiquitinatio
268 dler syndrome and also produces enlarged and hyperactive stem cell compartments, which lead to hypert
270 SGs, offering a potential avenue to mitigate hyperactive stress responses under pathological conditio
272 ion or risk variants in these genes revealed hyperactive T cell responses, whereas studies of human l
276 2%-24%]; P=0.016 for ejection fraction), and hyperactive TGFbeta signaling in transverse aortic const
277 cient T cells, exhibiting a dysregulated and hyperactive Th17 phenotype with overproduction of IL-22
278 m specifically denotes disorders involving a hyperactive thyroid gland (Graves disease, toxic multino
279 treme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Prob
281 ocytes of synthetic mRNA encoding the SB100X hyperactive transposase together with plasmid DNA carryi
282 o-injection of a plasmid encoding the SB100X hyperactive transposase, together with a second plasmid
284 myeloid cells, and blocking STING suppresses hyperactive type I interferon responses in C9orf72(-/-)
287 cs simulations that suggest that AID and its hyperactive variants can engage DNA in multiple specific
293 ppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on alpha-catenin;