ライフサイエンスコーパス: hyperactive

1 d L residues and found that the majority are hyperactive.

2 t mTOR activity, despite both pathways being hyperactive.

3 runcation of this domain renders the channel hyperactive.

4 sting GluN2B-containing NMDARs in the KO are hyperactive.

5 jections, could move effectively and even be hyperactive 72 h after the last L-DOPA injection when do

6 an mTORC1 activator and an oncogene and that hyperactive AA signaling through Rab1A overexpression dr

7 and somatic Ca(2+) imaging, we have observed hyperactive action-potential firing.

8 Hyperactive AFPs, identified in insects, have an especia

9 olved in the pathophysiology of ADs, becomes hyperactive after ethanol withdrawal.

10 a (PGC1alpha), which became deacetylated and hyperactive after oleic acid treatment.

11 Finally, using a hyperactive AID variant, we mutagenize loci both upstrea

12 ed that in PTEN-mutated endometrial cancers, hyperactive Akt signaling downregulates progesterone rec

13 Hyperactive Akt specifically activates TSC1-dependent cy

14 hyperresponsiveness in PTSD may arise from a hyperactive alerting/orienting system in which processes

15 show that common VCP disease mutants act as hyperactive alleles with respect to regulation of Mitofu

16 ymorphism Leu33Pro (rs5918, Pl(A2)) produces hyperactive alphavbeta3 receptors that influence whole-b

17 tors that mediate the detrimental effects of hyperactive AMPK in AD pathophysiology.

18 The results link hyperactive amygdala responses and regions critical for

19 of whom 51 (58.6%) were of mixed, 10 (11.5%) hyperactive and 26 (29.9%) hypoactive delirium subtypes.

20 ed individuals, especially those who exhibit hyperactive and anxiety-related symptoms.

21 Rictor CKO mice are hyperactive and have reduced anxiety-like behavior.

22 rons, both cell populations were found to be hyperactive and hyper-responsive to ATP.

23 inactivating mutations in GATOR1, mTORC1 is hyperactive and insensitive to amino acid starvation, an

24 ic neurons driven by Vgat-ires-Cre, both the hyperactive and lean phenotypes were completely correcte

25 ysis illustrates that BPA is associated with hyperactive and lean phenotypes.

26 ocyte-specific RIIbeta reexpression remained hyperactive and lean, but pan-neuronal RIIbeta reexpress

27 r that will provide a means for isolation of hyperactive and other interesting classes of transposase

28 t allele of Arabidopsis cry1 is biologically hyperactive and seems to mimic the ATP-bound state of cr

29 Larvae deprived of maternal rest are hyperactive and show atypical spatial preferences.

30 imension "overactivity." Ncan(-/-) mice were hyperactive and showed more frequent risk-taking and rep

31 behavioral problems consisting of autistic, hyperactive and/or aggressive behavior.

32 e; thus, mice lacking MCH or MCHR1 are lean, hyperactive, and resistant to diet-induced obesity.

33 that the common high risk Arg-325 variant is hyperactive, and thus may be targeted for inhibition to

34 a state of chronic decompensated HF, and the hyperactive ANS will continue to push the heart to work

35 ultaneous loop 3/7 replacement resulted in a hyperactive APOBEC3G variant that also preferred 5'-TC d

36 on site on AR results in a transcriptionally hyperactive AR, suggesting that the proliferative effect

37 Stable expression of truncated, hyperactive ASXL1-BAP1 complexes in a haematopoietic pre

38 in diseases in which the carotid bodies are hyperactive at rest, e.g. essential hypertension, obstru

39 potential therapeutic target for combatting hyperactive AURKA-driven NSCLCs.

40 but complete removal of the brake can induce hyperactive autoubiquitination and E3 self destruction.

41 signaling in B cells could therefore lead to hyperactive B cells and Ig overproduction.

42 ults in a lupus-like autoimmune disease with hyperactive B cells and myeloproliferation.

43 maintained, together with the suppression of hyperactive B cells.

44 The hyperactive B-cell responses are thought to underlie the

45 a role in satiation and attention deficiency/hyperactive behavior.

46 ly during the neurogenic window caused later hyperactive behaviors in zebrafish larvae.

47 iceptive dose-response (ED50) was tested and hyperactive behaviors such as jumping and scratching wer

48 bate morphine tolerance and morphine-induced hyperactive behaviors, and (2) protein kinase C (PKC) wo

49 midazolam also exacerbated morphine-induced hyperactive behaviors.

50 Hyperactive beta-catenin drives colorectal cancer, yet i

51 verexpressed in rat hippocampal neurons, the hyperactive BICD2 mutants decreased neurite growth.

52 we analyzed protein-protein interactions of hyperactive BRAF(V)(600E) and wild-type BRAF (BRAF(WT)).

53 Hyperactive BRAF(V)(600E) resides in large complexes of

54 k shows that the adolescent reward system is hyperactive, but this finding may be confounded by diffe

55 of R139W-C3 resulted from the formation of a hyperactive C3 convertase.

56 In Akt-hyperactive cancer, TopBP1 forms oligomers and represses

57 ndant inhibitory REs to achieve the level of hyperactive CARD11 signaling required to support lymphom

58 , in which 11 sites were mutated to Ala, was hyperactive, causing increased inward transport of phosp

59 Allergic diseases, orchestrated by hyperactive CD4(+) Th2 cells, are some of the most commo

60 e HLH phenotype was further characterized by hyperactive CD8 T cells and continuous IFN-gamma product

61 or for promoting cell death of uncontrolled, hyperactive CD8(+) T cells to prevent immunopathology.

62 We also provide evidence that hyperactive Cdc2.1w locks cells in a G1-like DNA repair

63 e here that fission yeast cells harbouring a hyperactive Cdc2CDK1 mutation (cdc2.1w) are specifically

64 ory protein, which inhibits Cdk5/p35 and the hyperactive Cdk5/p25 activities in test tube experiments

65 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

67 cause of congenital hyperinsulinism, whereas hyperactive channels are a cause of neonatal diabetes.

68 ctional driver lines consistently reproduced hyperactive climbing whereas strong or weak artificial d

69 cle, we show that DC from lpa2(-/-) mice are hyperactive compared with their wild-type counterparts a

70 at ENT1 KO mice were both active earlier and hyperactive compared with WT mice at night.

71 tal multi-organ autoimmunity associated with hyperactive conventional T cell responses and poor Treg-

72 ; however, our KO mice display evidence of a hyperactive counter-regulatory response rather than insu

73 This hyperactive COX-2/PGE2-induced suppression is evident du

74 Genetic depletion of TLR4 or SPAK normalizes hyperactive CSF secretion rates and reduces PHH symptoms

75 Hyperactive DCs are defined by their ability to release

76 tivation state, which we call "hyperactive." Hyperactive DCs induce potent adaptive immune responses

77 r on the domain mental health than mixed and hyperactive delirium patients.

78 % of delirium episodes were characterized as hyperactive delirium.

79 t of choice in adults with attention-deficit hyperactive disorder (ADHD) and some studies were conduc

80 s that high levels of SUN proteins lead to a hyperactive DNA damage response.

81 nd led to unrestrained DSB end resection and hyperactive DNA repair.

82 cells in vitro, which were attributed to the hyperactive DNMT1 or KIT, because inactivation of KIT or

83 Multiple readouts demonstrated hyperactive Dpp signaling in piwi mutants, including the

84 is that developing Pten-depleted neurons are hyperactive due to increased excitatory synaptogenesis u

85 Hyperactive EGF receptor (EGFR) and mutant p53 are commo

86 ac) was originally cloned as an inhibitor of hyperactive EGFR alleles.

87 ich half strongly interacted with oncogenic, hyperactive EGFR variants.

88 e mice became lean but ate normally and were hyperactive, especially during a fast.

89 ct reactivity and empathy in the presence of hyperactive executive control.

90 ike or depression-like behaviors, as well as hyperactive fear circuits, glucocorticoid receptor hyper

91 hyperacusis have been linked to abnormal and hyperactive firing patterns within the auditory system,

92 is was increased in mice expressing a mutant hyperactive form of CDK4 (CDK4(R24C)).

93 e all dominant and are proposed to result in hyperactive forms of the formaldehyde dehydrogenase enzy

94 RPs, young hyperactive forms, are increased during situations of en

95 f Fps1 from Saccharomyces cerevisiae and the hyperactive Fps1 ortholog from Ashbya gossypii.

96 39 was abrogated by both the expression of a hyperactive GAC(K320A) allele and the addition of the tr

97 glucokinase-deficient bacterium, uncovers a hyperactive GCK variant with substantially reduced coope

98 ses osteoblast-specific marker expression in hyperactive Gja1(Jrt)/+ osteoblasts and may also increas

99 ive in the mouse model of FXS (FX mice), and hyperactive GSK3 promotes locomotor hyperactivity and au

100 Furthermore, the age-dependent hyperactive GSK3beta caused a significant deficit in lon

101 n during cortical development, the transient hyperactive GSK3beta likely accounts for the cortical sp

102 We found that Nedd4-2 heterozygous mice are hyperactive, have increased basal synaptic transmission

103 Heterologous expression of these hyperactive heteromeric hemichannels increases cell memb

104 The influence of these hyperactive hippocampal projections on targets in the li

105 Hyperactive Hnf4 signaling leads to up-regulation of lip

106 genase mRNAs in the NTS, and this normalized hyperactive HPA axis responses to IL-1beta.

107 acutely to PNS rats overrides programming of hyperactive HPA axis responses to immune challenge in a

108 virus (AAV) that expresses a codon-optimized hyperactive human factor IX (FIX) mutant (FIX Padua), it

109 sponse DNA polymerase (Pol) lambda caused by hyperactive HUWE1 p.R4187C.

110 enhanced DC activation state, which we call "hyperactive." Hyperactive DCs induce potent adaptive imm

111 Hyperactive, hyperphosphorylated RyRs because of reduced

112 infiltration of lungs due to the presence of hyperactive immune cells.

113 that pathogenesis is appreciably driven by a hyperactive immune response.

114 Moreover, hyperactive immunity and increased enterocyte death resu

115 r the categorical disorder of ADHD influence hyperactive-impulsive and attentional traits in the gene

116 r executive inhibition deficiency related to hyperactive-impulsive behavior in ADHD, further emphasiz

117 For example, hyperactive-impulsive behavior scores at age 8 years wer

118 Active line represents a valid model for the Hyperactive-Impulsive subtype of ADHD and therefore may

119 Regressions of childhood inattentive and hyperactive-impulsive symptoms were conducted to predict

120 wed a positive association with ADHD traits (hyperactive-impulsive, p = .0039; inattentive, p = .037)

121 Furthermore, hyperactive-impulsive-like behavior was induced by reduc

122 trast to the general notion that dopamine is hyperactive in adolescents, there is diminished presynap

123 onsive genes are overrepresented among those hyperactive in arp6.

124 pk1 activity in vivo, we found that Fpk1 was hyperactive in cells lacking Gin4, a protein kinase prev

125 versive processing and is hypothesised to be hyperactive in depression, contributing to the generatio

126 in planta upon photoconversion to Pfr and is hyperactive in driving photomorphogenesis.

127 ndin-null neurons, dendritic protrusions are hyperactive in formation, retraction, and conversion bet

128 her peripheral and central chemoreflexes are hyperactive in HFpEF and if chemoreflex activation exace

129 zyme of the mevalonate pathway that is often hyperactive in malignant cells.

130 th this finding, Hippo signaling is markedly hyperactive in mammalian Dlg5(-/-) tissues and cells in

131 sting that the autophagy/lysosome pathway is hyperactive in motor neurons of SOD1-linked ALS mice.

132 hagy/lysosome pathway was either impaired or hyperactive in motor neurons, chloroquine was administer

133 t both Wnt and Notch signaling pathways were hyperactive in Mtgr1(-/-) tumors.

134 rtico-striatal-thalamic circuit is tonically hyperactive in mutants, but becomes hypoactive during so

135 yl arginine deiminases have been shown to be hyperactive in neurodegenerative diseases including mult

136 mTOR signaling is hyperactive in neurological syndromes in both humans and

137 Thus, activity in lOFC, which is known to be hyperactive in obsessive-compulsive disorder, may be res

138 ssed in the striatum, a brain region that is hyperactive in OCD.

139 t, Runx2 is activated by signals known to be hyperactive in PCa including the RAS/MAP kinase pathway,

140 ting alpha3DeltaN proteasomes are intact but hyperactive in the hydrolysis of fluorogenic peptide sub

141 CDK4/6 are rendered hyperactive in the majority of human cancers through a m

142 egulated kinase (ERK)1/2 signaling, which is hyperactive in the majority of melanomas.

143 ocampal glycogen synthase kinase-3 (GSK3) is hyperactive in the mouse model of FXS (FX mice), and hyp

144 , both Plxna4(+/-) and Plxna4(-/-) mice were hyperactive in the open field assay while Plxna4(-/-) mi

145 Both GSK-3 isozymes (alpha/beta) were hyperactive in this model.

146 on's disease, at an age when the neurons are hyperactive in vivo and the mice begin to exhibit locomo

147 e mutations in cryopyrin (NLRP3) result in a hyperactive inflammasome that drives overproduction of t

148 Deregulated and hyperactive inflammation contributes to tissue damage an

149 Impaired bacterial clearance and hyperactive innate immune response are hallmarks of the

150 ng that excessive nitric oxide released from hyperactive interneurons and glia inhibited vessel growt

151 vation of its expression contributes to both hyperactive intracellular Ca(2+) oscillations and fast c

152 ients with autoimmune arthritis demonstrated hyperactive intracellular complement activation and inte

153 These defects are suppressed by hyperactive IP(3) signaling, suggesting that C17ISO and

154 Hyperactive JAK/STAT and PI3K/mammalian target of rapamy

155 Hypertensive Cyp2c44(-/-) mice show a hyperactive kidney epithelial sodium channel (ENaC) and

156 or suppressor genes, whereas PKC412 inhibits hyperactive kinase signaling, which is essential for can

157 For P3a, hyperactive left PrCS was found in comorbid patients.

158 mportant to identify the mechanism governing hyperactive lipogenesis in malignant cells.

159 s complex genes (TSC1 or TSC2), resulting in hyperactive mammalian Target of Rapamycin (mTOR) signali

160 th the metastasis of tuberin-null cells with hyperactive mammalian target of rapamycin complex 1 (mTO

161 Hyperactive mammalian target of rapamycin complex 1 (mTO

162 malignancies, its utility as a suppressor of hyperactive MAPK signaling in the absence of mutated Raf

163 e therefore established an in vivo model for hyperactive mast cells by specifically ablating the NF-k

164 Our results provide in vivo evidence that hyperactive mast cells can exacerbate inflammatory disor

165 , SLC32A1) in histaminergic neurons produced hyperactive mice with an exceptional amount of sustained

166 A hyperactive MRP-1 system for GSSG efflux acts as a criti

167 Hyperactive MTOC function at the centrosome is associate

168 Considering that pathological hyperactive mTOR also occurs in individuals carrying no

169 Moreover, Fnip1(-/-) iNKT cells contained hyperactive mTOR and reduced mitochondrial number despit

170 n of eIF4E and its increased availability by hyperactive mTOR and to require phosphorylation of eIF4E

171 Abnormal axonal connectivity and hyperactive mTOR complex 1 (mTORC1) are shared features

172 nt of KS and other tumor lesions, exhibiting hyperactive mTOR pathway function.

173 However, whether hyperactive mTOR plays a role in the cognitive deficits

174 Our results implicate hyperactive mTOR signaling as a previous unidentified si

175 Furthermore, hyperactive mTOR signaling may represent a molecular pat

176 Importantly, increased mitotic activity and hyperactive mTOR signaling was also observed in recently

177 Hyperactive mTORC1 alters axon length and polarity of hi

178 pocampal neurons in vitro, but the impact of hyperactive mTORC1 on axon growth in vivo and the mechan

179 These include multiple indicators of hyperactive mTORC1 signaling, presence of specific neura

180 th mutations of MTOR, TSC1, TSC2 or PTEN and hyperactive mTORC1 signalling are associated with better

181 eases associated with mutations that lead to hyperactive mTORC1 signalling.

182 gic substrate that accumulates in cells with hyperactive mTORC1, such as kidney cells with mutations

183 ly rescuing dendritic hypertrophy induced by hyperactive mTORC1.

184 we developed transgenic mice that express a hyperactive mutant of Stat5 in hematopoietic progenitors

185 al therapeutic targets due to their frequent hyperactive mutations and overexpression found in cancer

186 valuable for studying the in vivo effects of hyperactive Nav1.6 and the response to therapeutic inter

187 Blocking hyperactive NCC in the DCT gradually restored ASDN struc

188 A decline in GABAAR signalling triggers hyperactive neurological disorders such as insomnia, anx

189 ough even restricted influx of Rho-deficient hyperactive neutrophils exacerbated lipopolysaccharide-m

190 by massive infiltration and sequestration of hyperactive neutrophils in the visceral organ.

191 log of D303N in human NLRP3), resulting in a hyperactive NLRP3.

192 rtially restored patterning, suggesting that hyperactive Nodal signalling contributes to the gastrula

193 Ptch2(-/-) niche cells show hyperactive noncanonical HH signaling, resulting in redu

194 Conversely, dSPNs were neither hyperactive nor synchronized to a large extent during co

195 velopment and in adult tissues, and aberrant hyperactive Notch signaling causes some forms of cancer.

196 w analogous honeycomb cysts with evidence of hyperactive Notch signalling.

197 of the CDKN2A/2B cell-cycle regulators, and hyperactive NOTCH1 signaling play prominent roles in the

198 erma, lymphoproliferation, elevated IgE, and hyperactive oligoclonal T cells.

199 Such hyperactive OPS versions can even complement the severe

200 are largely due to inappropriate response of hyperactive or autoreactive B cells.

201 Four gain-of-function mutations that form a hyperactive or deregulated C3 convertase have been ident

202 ers can, depending on cancer type, be either hyperactive or inactivated.

203 Hospitalized patients experiencing hyperactive or mixed delirium and receiving continuous o

204 Hyperactive or mixed delirium is a common and serious co

205 Hfe(-/-) x Tfr2(mut) mice were hyperactive (P<0.0112) without apparent cognitive impair

206 er, exposure to sublethal stress resulted in hyperactive p53 and p53-dependent mortality in Mdm2(Y487

207 The end result is a hyperactive pathway, initiated by progesterone and ampli

208 A hyperactive PB (hyPB) transposase was then deployed to e

209 Hyperactive performance monitoring, as measured by the e

210 CD300f-deficient dendritic cells displayed hyperactive phagocytosis of apoptotic cells, which stimu

211 T cells of CYLD(ex7/8) mice had a hyperactive phenotype manifested by increased production

212 tabolically, the DeltascmR strain displays a hyperactive phenotype relative to wild type and overprod

213 cell development confers these cells with a hyperactive phenotype.

214 treat mania associated with BD, rescued the hyperactive phenotypes of Plcg1(f/f); CaMKII mice.

215 rozygosity for a Pten null allele to promote hyperactive PI3K/AKT signaling.

216 on insertions by comparing a series of novel hyperactive piggyBac constructs tethered to a custom tra

217 entiviral particles (LPs) as carriers of the hyperactive piggyBac transposase protein (hyPBase), we d

218 on (PNI) technique described herein uses the hyperactive piggyBac transposase to insert a large trans

219 Hyperactive piggyBac transposon is particularly promisin

220 a genetic screen is used to identify several hyperactive point mutations, which are then incorporated

221 Remarkably, induction of a hyperactive PP1/NIPP1 holoenzyme, further shifted direct

222 alysis from TCGA raised the possibility that hyperactive PPAR signaling, either due to PPAR gamma gen

223 e, suggesting that the mutant alleles encode hyperactive PPM1D isoforms.

224 Moreover, miRNA biomarkers of hyperactive PR-A may help predict metastatic potential o

225 Itk(-/-)Btk(-/-) mast cells exhibit hyperactive preformed and LPS-induced TNF-alpha producti

226 Anxious patients demonstrated hyperactive prefrontal cortices (PFC).

227 Cells expressing the hyperactive proteasomes show markedly elevated degradati

228 lycemic index foods may lead to a hormonally hyperactive proximal gut and a hypoactivate distal gut,

229 r developing strategies to selectively block hyperactive RAS function.

230 t specific pathways mediating the effects of hyperactive Ras in NF1 tumors are unknown.

231 NF1 tumor suppressor gene function, causing hyperactive Ras signaling.

232 and patient-derived GBM specimens exhibiting hyperactive Ras.

233 n by a previously 'undruggable' oncogenic or hyperactive Ras.

234 nsitive to granulocyte macrophage-CSF due to hyperactive RAS/ERK signaling.

235 hat Sprouty gene loss-of-function results in hyperactive RAS/ERK1/2 signaling throughout the prostate

236 ated inflammation, Act1-deficient mice had a hyperactive response of the T(H)17 subset of helper T ce

237 The variations were seen as a hyperactive response subtype that showed elevated activa

238 However, in contrast to spontaneous hyperactive responses reported previously, the cells dis

239 evations in D2/3 receptor availability and a hyperactive reward processing network, underlies mania.

240 The onco-Lbc protein is a hyperactive Rho-specific guanine nucleotide exchange fac

241 -) DCs is supported by integrin CD11b and by hyperactive RhoA.

242 Hyperactive ribosomal biogenesis is widely observed in c

243 Specifically, hypoactive medial OFC and hyperactive right hippocampus responses to stress were e

244 ed by spontaneous Ca(2+) release events from hyperactive ryanodine receptor type 2 channels.

245 Hyperactive RyR2 channels directly stimulated the Ca(2+)

246 Hence, hyperactive RyR2 channels eager to release Ca(2+) on the

247 y, we demonstrated that AID mutations caused hyperactive Set2 in vivo and displayed a synthetic inter

248 Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcrip

249 sted that reinforcing feedback is central to hyperactive signaling in a diversity of cell fate progra

250 voked Ca(2+) signals by PGE2 occurs through "hyperactive signaling junctions," wherein cAMP is locall

251 pressors of a sluggish phenotype caused by a hyperactive SLO-2.

252 Gain-of-function experiments show that hyperactive small GTPase Kras expands the branching prog

253 tion of the C-terminal region also creates a hyperactive SMARCAL1 protein suggesting that S889 phosph

254 sed TORC1 activity, whereas cells containing hyperactive Snf1 display a PAS kinase-dependent decrease

255 ith marked cortical pathology, we found that hyperactive somatostatin interneurons disinhibited layer

256 Hyperactive STAT3 is thought to be oncogenic in PCa.

257 Downregulation of hyperactive Stat5 in diseased animals restored normal gr

258 change (hysteresis) and gradually attains a hyperactive state in which it is more active than it was

259 bilization of enzymes by ligand binding: the hyperactive state is only reached through ATP hydrolysis

260 g deconjugation of NEDD8 traps the CRLs in a hyperactive state, thereby leading to auto-ubiquitinatio

261 estricting branching does not produce a more hyperactive state.

262 proposed as a key mechanism underlying this hyperactive state.

263 ing cIAP1-targeted therapies to correct NOD2-hyperactive states and identifies a ubiquitin-regulated

264 dler syndrome and also produces enlarged and hyperactive stem cell compartments, which lead to hypert

265 Hyperactive Syk was functionally equivalent to acute act

266 ped spontaneous autoimmunity associated with hyperactive T cells, with increased production of IFN-ga

267 Introduction of a hyperactive TEL1-hy mutation suppressed the tel1-21 muta

268 an be exchanged, we show that the binding of hyperactive Tenebrio molitor AFP to ice crystals is prac

269 Because hyperactive TG2 is thought to play a role in various dis

270 Zhang et al. identify hyperactive TGF-beta signaling as an underlying cause of

271 mice was associated with immunopathology and hyperactive Th1 cell function as revealed by enhanced IF

272 cient T cells, exhibiting a dysregulated and hyperactive Th17 phenotype with overproduction of IL-22

273 The hyperactive Th17 response combined with fully responsive

274 B cells from these mice are hyperactive to antigen-receptor stimulation owing to a l

275 treme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Prob

276 lymerase chain reaction (PCR) array revealed hyperactive transforming growth factors beta/bone morpho

277 auty (SB) transposon system using the SB100X hyperactive transposase to transduce human cord blood CD

278 ocytes of synthetic mRNA encoding the SB100X hyperactive transposase together with plasmid DNA carryi

279 o-injection of a plasmid encoding the SB100X hyperactive transposase, together with a second plasmid

280 ection of synthetic mRNA encoding the SB100X hyperactive transposase, together with circular plasmid

281 taneous microvascular thrombosis by cleaving hyperactive ultra large von Willebrand factor multimers

282 pha-granules of platelets and is enriched in hyperactive "ultra-large" VWF multimers.

283 signaling screen that identifies new CARD11 hyperactive variants and defines a LATCH domain that fun

284 cs simulations that suggest that AID and its hyperactive variants can engage DNA in multiple specific

285 ate genetics have spurred efforts to develop hyperactive variants.

286 ecent laboratory experiments, we find that a hyperactive waveform does result in frequent detaching a

287 The second, hyperactive, waveform is classified by vigorous asymmetr

288 A phosphomimetic S889 mutant is also hyperactive when expressed in cells, while a non-phospho

289 rates (Sla1 and Ent2) confirmed that Akl1 is hyperactive when not phosphorylated by Fpk1.

290 Here we show that ATM is hyperactive when the catalytic subunit of DNA-dependent

291 research has suggested that the Wistar-Kyoto Hyperactive (WKHA) rat strain may model some of the beha

292 ppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on alpha-catenin;

293 Hyperactive Wnt signaling is frequently observed in colo

294 In a hyperactive WNT signaling mouse model of human osteoscle

295 macrophage subsets, increased proliferation, hyperactive WNT signaling, and increased DNA damage.

296 rgets it for degradation under conditions of hyperactive Wnt signaling.

297 esting and stimulated conditions, suggesting hyperactive Wnt signaling.

298 Hyperactive Wnt/beta-catenin signaling is linked to canc

299 Hyperactive YB-1 and Ape/Ref-1 were responsible for high

300 autoinhibitory mechanism, producing a weakly hyperactive ZAP-70 protein.