ライフサイエンスコーパス: hyperphosphorylation

1 than viral replication via mediation of NS5A hyperphosphorylation.

2 ich is important for CKI-alpha-mediated NS5A hyperphosphorylation.

3 cell survival, which is correlated with BAD hyperphosphorylation.

4 characterized by detergent insolubility and hyperphosphorylation.

5 , synaptic loss, Abeta accumulation, and tau hyperphosphorylation.

6 ed to assess amyloid beta deposition and tau hyperphosphorylation.

7 of p107 while B55alpha knockdown results in hyperphosphorylation.

8 also inhibits Dishevelled1-induced Frizzled3 hyperphosphorylation.

9 ined, but young NOD mice did not display tau hyperphosphorylation.

10 es amyloid beta (Abeta) accumulation and tau hyperphosphorylation.

11 ed CDK9 as a potential kinase mediating BRD4 hyperphosphorylation.

12 on is by inactivation of pocket proteins via hyperphosphorylation.

13 le the trans-acting function likely requires hyperphosphorylation.

14 prolonged stress may increase Abeta and tau hyperphosphorylation.

15 u-dependent loss of dendritic spines and tau hyperphosphorylation.

16 on between TORC2 and Gad8 and to induce Gad8 hyperphosphorylation.

17 ension and hyperkalemia, concurrent with NCC hyperphosphorylation.

18 impairment, abnormal APP processing and tau hyperphosphorylation.

19 SF1 leads to enhanced TDP-43 aggregation and hyperphosphorylation.

20 expression of PITX1 and p120RasGAP by PITX1 hyperphosphorylation.

21 affected by the presence of the PRR and tau hyperphosphorylation.

22 vity is regulated by ERK2- and Cdk1-mediated hyperphosphorylation.

23 We previously showed that topo I hyperphosphorylation, a cancer-associated event mediated

24 IP reduced pathologic changes, including tau hyperphosphorylation, (Abeta) deposit, astrocytosis, and

25 However, how its hyperphosphorylation affects cardiac function in vivo re

26 the nuclear export signal of CHK1 led to its hyperphosphorylation after irradiation and reduced centr

27 Topo I hyperphosphorylation also increases its interaction with

28 ions affecting serine residues important for hyperphosphorylation and a subset of the domain I mutati

29 the mutant tau in MEC induces endogenous tau hyperphosphorylation and accumulation in hippocampus and

30 c1 single-mutant mice with rapamycin reduced hyperphosphorylation and accumulation of 4E-BP1 but also

31 ubules in neurons, but in diseased cells tau hyperphosphorylation and aggregation are evident and com

32 First, tau hyperphosphorylation and aggregation occur as early as 2

33 veral transgenic animal models of LRRK2, tau hyperphosphorylation and aggregation, rather than alpha-

34 was associated with more severe neuritic tau hyperphosphorylation and axonal dystrophy around amyloid

35 Similar tau hyperphosphorylation and CCE are typical features of neu

36 f transcription 1 levels and gliosis, and 2) hyperphosphorylation and conformational alterations of s

37 rom various experimental models suggest that hyperphosphorylation and conformational changes of tau c

38 pamycin complex 1 (mTORC1) signaling causing hyperphosphorylation and consequent accumulation of 4E-B

39 ta-catenin degradation complex, favoring the hyperphosphorylation and degradation of beta-catenin.

40 Furthermore, blockage of CMA leads to hyperphosphorylation and destabilization of the MRN (Mre

41 functions of Vangl2 and Dvl1 (over Frizzled3 hyperphosphorylation and endocytosis) allow sharpening o

42 ation between the temporal profile of STEP61 hyperphosphorylation and ERK2 phosphorylation indicates

43 a linker domain in protein constructs allows hyperphosphorylation and further enhancement of RNase ac

44 hanges in MRI, neurobiochemical markers (Tau hyperphosphorylation and glia activation in brain tissue

45 sequence I of NS5A that is involved in NS5A hyperphosphorylation and hyperphosphorylation-dependent

46 n NS5A (genotype 2a) may be involved in NS5A hyperphosphorylation and hyperphosphorylation-dependent

47 rylation, characterized by epitope-dependent hyperphosphorylation and hypophosphorylation, correlated

48 tigated whether HD pathology may promote tau hyperphosphorylation and if so tackle some of its underl

49 es that were examined, also leading to Ser-5 hyperphosphorylation and increased ubiqutination within

50 s an NS5A-associated kinase involved in NS5A hyperphosphorylation and infectious virus production.

51 cRyr2Delta50 hearts exhibited hyperphosphorylation and inhibition of pyruvate dehydrog

52 cAMP and, to some extent, cGMP to induce the hyperphosphorylation and insolubility of endothelial Tau

53 , we observed a positive correlation between hyperphosphorylation and JFH1 replicon replication.

54 elled2 blocks Dishevelled1-induced Frizzled3 hyperphosphorylation and membrane accumulation.

55 s disease, including amyloid production, tau hyperphosphorylation and memory loss.

56 europathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spine

57 r indirectly, and prevents Abeta-induced tau hyperphosphorylation and mitochondrial fragmentation.

58 ic plasticity, decrease synapses, induce tau hyperphosphorylation and neuritic dystrophy, activate mi

59 , this experience also reduces levels of tau hyperphosphorylation and oligomeric beta-amyloid.

60 Hodgkin lymphoma cell line KM-H2 resulted in hyperphosphorylation and overexpression of downstream on

61 Notably, tau hyperphosphorylation and potentiation of amyloidogenic p

62 e nucleus on serine 183, which catalyzes its hyperphosphorylation and proteosomal degradation.

63 attenuated amyloid beta accumulation and tau hyperphosphorylation and rescued hippocampal LTP and mem

64 activation during IR prevented AMPK(Ser-485) hyperphosphorylation and restored AMPK-mediated Tau deph

65 reticulum Ca2+ load related to phospholamban hyperphosphorylation and ryanodine receptor dysregulatio

66 extracts two measures of Cdc25C activation (hyperphosphorylation and Ser 287 dephosphorylation) are

67 f Akt may prove beneficial in preventing tau hyperphosphorylation and subsequent neuropathology in AD

68 in mitochondria proteome appeared before tau hyperphosphorylation and tangle formation, which were ob

69 the human tau mutated gene, resulting in tau hyperphosphorylation and tangle formation.

70 s an NS5A-associated kinase involved in NS5A hyperphosphorylation and the production of infectious vi

71 Furthermore, Pin4C aggregation, hyperphosphorylation and toxicity are simultaneously rev

72 mutagenesis from MCV sT LSD-dependent 4E-BP1 hyperphosphorylation and viral DNA replication enhanceme

73 Abnormal phosphorylation ("hyperphosphorylation") and aggregation of Tau protein ar

74 howed that phosphorylation at S146 regulates hyperphosphorylation, and by generating a phospho-specif

75 ere able to induce marked neuronal loss, tau hyperphosphorylation, and deficits in hippocampus-depend

76 e HFpEF, LA cardiomyocyte hypertrophy, titin hyperphosphorylation, and microvascular dysfunction occu

77 bilizing tau function, caused by misfolding, hyperphosphorylation, and sequestration of tau into inso

78 ally believed that beta-amyloidogenesis, tau-hyperphosphorylation, and synaptic loss underlie cogniti

79 Here we present evidence for hyperphosphorylation as a mechanism allowing UPF1, the c

80 This is not due to RPA2 hyperphosphorylation as suppression of this response doe

81 on the cell surface and displayed a pan-STAT hyperphosphorylation associated with acquisition of a di

82 of AD pathology, including synapse loss, tau hyperphosphorylation, astrocyte and microglial activatio

83 nal changes in the N-terminal region lead to hyperphosphorylation at C-terminal sites, which seem not

84 y decreased brain Abeta accumulation and Tau hyperphosphorylation at multiple AD relevant epitopes.

85 mice, whereas symptomatic mice displayed tau hyperphosphorylation at multiple tau phosphoepitopes (AT

86 au kinase activity resulting in elevated tau hyperphosphorylation at PP2A favorable sites.

87 ctivation; elevated APAP protein adducts; K8 hyperphosphorylation at S74/S432 with enhanced keratin s

88 However, we find consistent hyperphosphorylation at serine 380 of PTEN, which is an

89 We found that hyperphosphorylation at serine 5 of the C-terminal domai

90 Tau P301S) with (-)-nilvadipine reduces Tau hyperphosphorylation at several Alzheimer disease (AD) p

91 u-immunoreactive cell groups also showed tau hyperphosphorylation at the epitopes Thr231/Ser235 and S

92 We found a significant increase in tau hyperphosphorylation at the PHF-1 epitope in pre-symptom

93 rotein underwent massive degradation without hyperphosphorylation at three sites known to control E2F

94 ypothesize that these compounds decrease tau hyperphosphorylation based on the maintenance of the Ser

95 Moreover, the ability of UPF1 to undergo hyperphosphorylation becomes increasingly important for

96 zation of phosphomutants, we show that Cdc25 hyperphosphorylation by Cdk1 governs Cdc25 catalytic act

97 e blockage of the effect of gambierol on tau hyperphosphorylation by glutamate receptor antagonists.

98 Moreover, suppressing tau hyperphosphorylation by kinase inhibition nearly prevent

99 Importantly, IE1 hyperphosphorylation coincided exclusively with AcMNPV D

100 n regulates tau-microtubule interactions and hyperphosphorylation contributes to the aberrant formati

101 Hyperphosphorylation correlated with increased SfIAP tur

102 e of the two SPBs during anaphase, and Cdc11 hyperphosphorylation correlates with proficient SIN acti

103 cts such as increased levels of aggregation, hyperphosphorylation, defects in mRNA splicing, and weak

104 usly demonstrated trans-complementation of a hyperphosphorylation-deficient, replication-defective JF

105 Rb hyperphosphorylation, degradation, and binding by viral

106 This hyperphosphorylation-dependent feedback mechanism may se

107 is involved in NS5A hyperphosphorylation and hyperphosphorylation-dependent regulation of infectious

108 be involved in NS5A hyperphosphorylation and hyperphosphorylation-dependent regulation of virion prod

109 signaling is impaired, suggesting Frizzled3 hyperphosphorylation does correlate with loss of PCP sig

110 Simulation of disease-like tau hyperphosphorylation dramatically diminished the tau-MT

111 he CDK activities that maintain p130 and pRB hyperphosphorylation for several hours after p107 dephos

112 cytoskeletal proteins, cdk5 activation, tau hyperphosphorylation, formation of potentially neurotoxi

113 ay is demonstrated by measuring the state of hyperphosphorylation from tau in a cellular model for AD

114 iabetic NOD mice became hypothermic, and tau hyperphosphorylation further extended to paired helical

115 onic overactivation of Akt --> AMPK(Ser-485) hyperphosphorylation --> inhibition of AMPK-mediated Tau

116 Calpain activation and tau hyperphosphorylation have been implicated in both TBI an

117 r preventing both Abeta accumulation and Tau hyperphosphorylation in AD.

118 s to beta-amyloid (Abeta) production and tau hyperphosphorylation in Alzheimer's disease (AD).

119 esults do not support the importance of RyR2 hyperphosphorylation in Ca(2+)-dependent heart disease,

120 nous Abeta oligomer, Fyn alteration, and tau hyperphosphorylation in cellular and animal models model

121 reversible, apical trafficking but did block hyperphosphorylation in hepatic cells.

122 onmental neurotoxin on PP2A activity and tau hyperphosphorylation in mouse primary neuronal cultures

123 us calcineurin was sufficient to promote tau hyperphosphorylation in neuronal cells.

124 We induced tau hyperphosphorylation in organotypic hippocampal slice cu

125 e, we show that CtIP undergoes ATR-dependent hyperphosphorylation in response to DSBs.

126 are subject to ShcD-induced, cell-autonomous hyperphosphorylation in the absence of external stimuli.

127 e, including a tau isoform imbalance and tau hyperphosphorylation in the absence of somatodendritic t

128 dysfunction in NOD mice leads to AD-like tau hyperphosphorylation in the brain, with molecular mechan

129 Here, we investigated the role of RPA2 hyperphosphorylation in the fate of cells when CHK1 is i

130 pe I JAK2 inhibitors induce paradoxical JAK2 hyperphosphorylation in these leukemias and have limited

131 at mutant huntingtin can induce abnormal tau hyperphosphorylation in vivo, via the deregulation of ca

132 des an explanation for the "paradoxical" Akt hyperphosphorylation induced by ATP-competitive inhibito

133 ociated with end resection proficiency: CtIP hyperphosphorylation induced by Cpt and BRCA1 IRIF.

134 olished Fyn activation and Fyn-dependent tau hyperphosphorylation induced by endogenous oligomeric Ab

135 Interestingly, AKT hyperphosphorylation induced by GWL is independent of en

136 Cyclin E-mediated Rb hyperphosphorylation induces E2F transcriptional activat

137 In PS19 mice, RI stress promoted tau hyperphosphorylation, insoluble tau aggregation, neurode

138 the P301S mutation (PS19) that displays tau hyperphosphorylation, insoluble tau inclusions and neuro

139 BRD4 hyperphosphorylation is also observed in other cancers d

140 In the microtubule-associated protein tau, hyperphosphorylation is associated with protein misfoldi

141 , and cell culture studies revealed that tau hyperphosphorylation is caused by multiple factors, incl

142 to the widely held notion that aberrant Tau hyperphosphorylation is central to these disorders.

143 Hyperphosphorylation is deleterious to glycogen structur

144 Frizzled3 hyperphosphorylation is increased in Celsr3 mutant mice,

145 ossibly other tauopathies where aberrant tau hyperphosphorylation is involved.

146 but the mechanism by which BMAA leads to tau hyperphosphorylation is not known.

147 Since BMS-790052 also impairs JFH1 NS5A hyperphosphorylation, it likely also blocks the trans-ac

148 encoding AEP show substantially reduced tau hyperphosphorylation, less synapse loss and rescue of im

149 to a variety of animal models decreases Tau hyperphosphorylation, lowers brain amyloid plaque load,

150 One prevalent hypothesis is that hyperphosphorylation, misfolding, and fibrillization of

151 od agreement with previous observations that hyperphosphorylation negatively affects replication.

152 ated to the Abeta accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammati

153 n formation and provides novel insights into hyperphosphorylation observed in disease.

154 We showed that hyperphosphorylation occurs even when ATP7B is restricte

155 K8 hyperphosphorylation occurs in association with liver in

156 f HIV-infected cells confirmed Vif-dependent hyperphosphorylation of >200 cellular proteins, particul

157 owth factor-beta signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosp

158 Hyperphosphorylation of a serine-rich motif immediately

159 rexpression of Pin4C is deadly and linked to hyperphosphorylation of aggregated Pin4C.

160 conferred resistance to PLX4720 and induced hyperphosphorylation of AKT (v-akt murine thymoma viral

161 GISTs from cKit(V558Delta/+) mice confirmed hyperphosphorylation of AKT and ERK, but both remain unp

162 -1, but fail to recruit IkappaBs, results in hyperphosphorylation of alternative IKKbeta substrates.

163 Hyperphosphorylation of APC/C subunits, notably Apc1 and

164 ion of the Atg1-Atg13-Atg17 complex, through hyperphosphorylation of Atg13.

165 We found abnormal hyperphosphorylation of catenin delta-1 S268, which was

166 KC inhibitor, previously shown to affect the hyperphosphorylation of CELF1 and ameliorate the cardiac

167 Slow transcription also evoked a hyperphosphorylation of CTD Ser2 residues at 5' ends of

168 Hyperphosphorylation of DDR proteins is induced by up-re

169 Finally, hyperphosphorylation of endogenous full-length Pin4 was

170 Instead, loss of PHD3 results in hyperphosphorylation of epidermal growth factor receptor

171 Signaling studies revealed hyperphosphorylation of eukaryotic translation initiatio

172 led1 can inhibit PCP signaling by increasing hyperphosphorylation of Frizzled3 and preventing its int

173 ic fragments but does not involve or require hyperphosphorylation of full-length Tau.

174 r, mutant subunit overexpression resulted in hyperphosphorylation of GSK3beta, a B56delta-regulated s

175 , LCMT-1 homozygous knock-out MEFs exhibited hyperphosphorylation of HDAC3, a reported target of the

176 Hyperphosphorylation of IkappaB-alpha was observed in ma

177 alpha (PP2Acalpha) phosphatase resulting in hyperphosphorylation of inhibitory serine-166 and serine

178 maturely from the nucleolus concomitant with hyperphosphorylation of its nucleolar anchor protein Net

179 ncreased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myos

180 serine residues were important for efficient hyperphosphorylation of JFH1 NS5A.

181 on of beta-amyloid (Abeta) and intraneuronal hyperphosphorylation of microtubule-associated protein t

182 disassembles during mitosis, coincident with hyperphosphorylation of Mto2 protein.

183 F-H from AD brain and suggests that aberrant hyperphosphorylation of neuronal intermediate filament p

184 copy analyses showed that CKI-alpha-mediated hyperphosphorylation of NS5A contributes to the recruitm

185 CKI-alpha-dependent hyperphosphorylation of NS5A plays a role in recruiting

186 toplasmic trafficking by triggering aberrant hyperphosphorylation of nuclear pore proteins (Nup).

187 leocytoplasmic trafficking (NCT) by inducing hyperphosphorylation of nuclear pore proteins.

188 nt growth and tumor formation, and triggered hyperphosphorylation of oncogenic PP2A-B56/B' substrates

189 Myriocin-induced hyperphosphorylation of Orm1 and Orm2 does not occur in

190 cophenolate mofetil (Cellcept) modulated the hyperphosphorylation of P65 in B cells of RRMS patients

191 Unopposed cAMP stimulated hyperphosphorylation of PC2 in the absence of functional

192 -regulated the PITX1-p120RasGAP axis through hyperphosphorylation of PITX1.

193 Lastly, LPS and eritoran caused hyperphosphorylation of PKCzeta in a CD14-dependent and

194 rference-mediated silencing of CPL4 promoted hyperphosphorylation of pol II.

195 HF and CHF mice showed hyperphosphorylation of protein kinase A sites and the p

196 fly embryos with ionizing radiation leads to hyperphosphorylation of Psf2 subunit in the active helic

197 ON 01910.Na caused hyperphosphorylation of RanGAP1.SUMO1 within 4 hours tha

198 appears to rely on prolonged phosphorylation/hyperphosphorylation of RanGAP1.SUMO1.

199 sensitive to crosslinking agents and display hyperphosphorylation of Replication Protein A due to inc

200 sive stiffness, but this effect is offset by hyperphosphorylation of residues in titin spring element

201 n cyclin D1-CDK4 complex and p21 resulted in hyperphosphorylation of retinoblastoma protein at serine

202 ed during ETI, probably through CKI-mediated hyperphosphorylation of retinoblastoma-related 1 (RBR1).

203 eaks, activation of the ATM-CHK2 pathway and hyperphosphorylation of RPA.

204 Ca(2+) release and with a prevention of the hyperphosphorylation of ryanodine receptors under isopro

205 ease in wt-PMI cardiomyocytes was related to hyperphosphorylation of ryanodine receptors, which was b

206 hosphate-dependent protein kinase A-mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24,

207 s supporting this hypothesis have associated hyperphosphorylation of RyRS2808 and heart failure progr

208 CD160 in a human NK cell line, causing rapid hyperphosphorylation of serine kinases ERK1/2 and AKT an

209 Hyperphosphorylation of signal transducer and activator

210 This was associated with hyperphosphorylation of signaling proteins and enhanced

211 CDK5-mediated hyperphosphorylation of SIRT1 facilitates the developmen

212 crease in proliferation rate associated with hyperphosphorylation of Smad1/5/8.

213 RNA-mediated knockdown of TULA-2 resulted in hyperphosphorylation of spleen tyrosine kinase following

214 iBECs display hyperphosphorylation of STAT3 and STAT5 downstream of th

215 ese findings provide novel insights into the hyperphosphorylation of STAT3 in development of HNC.

216 over, Akt hyperactivation was accompanied by hyperphosphorylation of substrates glycogen synthase kin

217 Ablation of TULA-2 resulted in hyperphosphorylation of Syk and its downstream effector

218 tissue from these mice revealed a pronounced hyperphosphorylation of synaptic vesicle cycling protein

219 Hyperphosphorylation of tau and imbalanced expression of

220 ulation of GSK-3beta and consequent abnormal hyperphosphorylation of tau and neurofibrillary degenera

221 priate activation of Cdk5 and contributes to hyperphosphorylation of tau and other substrates that ar

222 treatment also attenuated anesthesia-induced hyperphosphorylation of tau and promoted the expression

223 nanomolar concentrations, they first induced hyperphosphorylation of tau at AD-relevant epitopes in h

224 tein expression, and this is associated with hyperphosphorylation of tau at serine-214.

225 l model (Tet-Off system) of AD-type abnormal hyperphosphorylation of Tau by expressing I2 (PP2A) in w

226 lytic subunit PP2Ac at Tyr(307) and abnormal hyperphosphorylation of tau in brains of patients who ha

227 aused GSK-3beta truncation at C-terminus and hyperphosphorylation of tau in mouse brain.

228 Molecular mechanisms leading to hyperphosphorylation of Tau in pathological conditions a

229 ake, transient activation of Tau kinases and hyperphosphorylation of Tau in the striatum were also ob

230 Hyperphosphorylation of tau is found within dystrophic n

231 Abnormal hyperphosphorylation of tau is pivotally involved in the

232 Abnormal hyperphosphorylation of Tau leads to the formation of ne

233 pes such as amyloid beta peptide production, hyperphosphorylation of tau protein and endosomal abnorm

234 Abnormal hyperphosphorylation of tau protein is a characteristic

235 Recent studies have demonstrated that hyperphosphorylation of tau protein plays a role in neur

236 loss of synapses and spines associated with hyperphosphorylation of tau protein.

237 een I2 (PP2A)-induced inhibition of PP2A and hyperphosphorylation of Tau that can be utilized to deve

238 Although local hyperphosphorylation of tau was increased in the dentate

239 impaired at the embryonic stage, even though hyperphosphorylation of tau was not detectable in these

240 ein phosphatase 2A (PP2A) activity, abnormal hyperphosphorylation of tau, and neurodegeneration; litt

241 ), inhibition of protein phosphatase 2A, and hyperphosphorylation of Tau, and the knockdown of aspara

242 -induced inhibition of PP2A and the abnormal hyperphosphorylation of tau, indicating the involvement

243 rrant activation of cdk5 and causes abnormal hyperphosphorylation of tau, thus leading to the formati

244 ion of PP2A was associated with the abnormal hyperphosphorylation of Tau, which resulted in microtubu

245 of beta-amyloid (Abeta) aggregation and the hyperphosphorylation of tau.

246 K3beta) may be critical for the pathological hyperphosphorylation of tau.

247 t kinase 5 (CDK5) and thereby diminished the hyperphosphorylation of tau.

248 y increased production of amyloid-beta42 and hyperphosphorylation of tau.

249 increased Src kinase activity and subsequent hyperphosphorylation of the actin regulator Cortactin.

250 In PTPN23-depleted tumors, we detected hyperphosphorylation of the autophosphorylation site tyr

251 AbetaOs also stimulate hyperphosphorylation of the axonal microtubule-associate

252 cal analysis of CD148-deficient ASM revealed hyperphosphorylation of the C-terminal inhibitory tyrosi

253 ompanied by activation of cAMP signaling and hyperphosphorylation of the dopamine- and cAMP-regulated

254 determined that these defects are caused by hyperphosphorylation of the inhibitory C-terminal tail o

255 Osmotic stress induced hyperphosphorylation of the mitotic inducer Cdr1 for sev

256 creases invasive capacities of cells through hyperphosphorylation of the oncogenic kinase AKT.

257 lation of the titin N2-B unique sequence and hyperphosphorylation of the PEVK (titin domain rich in p

258 as been proposed that protein kinase A (PKA) hyperphosphorylation of the RyR2 at a single residue, Se

259 used a mouse model (RyRS2808A) in which PKA hyperphosphorylation of the RyR2 at Ser-2808 is prevente

260 7 lytic genes during latency, leading to the hyperphosphorylation of the serine 5 residue and the hyp

261 ies revealed that GSK3 inhibition led to the hyperphosphorylation of the vitamin D receptor (VDR), en

262 nhanced association with WT EGFR, leading to hyperphosphorylation of the WT counterpart.

263 s in response to JNK activation and that the hyperphosphorylation of these sites renders the Rafs and

264 Hyperphosphorylation of this serine in cTnI C terminus i

265 n of the two mutations does not increase tau hyperphosphorylation or aggregation nor does it exacerba

266 eptidase-I2(PP2A)-protein phosphatase 2A-Tau hyperphosphorylation pathway as a therapeutic target.

267 Our data indicate that RPA2 hyperphosphorylation promotes cell death during replicat

268 red mouse locus coeruleus neurons expressing hyperphosphorylation-prone mutant human tau had shorter

269 y inducing a cascade of events including tau hyperphosphorylation, proteasome impairment, and synapti

270 To determine whether RPA2 hyperphosphorylation protects stalled forks from collaps

271 Overexpression of MARK4 led to tau hyperphosphorylation, reduced expression of synaptic mar

272 e opposite effects on APP processing and Tau hyperphosphorylation, relevant to the pathogenesis of AD

273 The functional significance of hyperphosphorylation remains unclear.

274 This stress-induced hyperphosphorylation required both Cdr1 autophosphorylat

275 characterized by MAP hypophosphorylation and hyperphosphorylation, respectively.

276 tion of gamma-secretase pathway, whereas tau hyperphosphorylation resulted from an activation of the

277 The underpinnings of STAT3 hyperphosphorylation resulting in enhanced signaling and

278 tiation factor 4E-binding protein 1 (4E-BP1) hyperphosphorylation, resulting in dysregulated cap-depe

279 Only PKCbeta inhibition resulted in Syk hyperphosphorylation similar to that in platelets treate

280 viruses displayed a markedly decreased NS5A hyperphosphorylation state (NS5A p58) relative to JFH1,

281 reduced basal phosphorylation and eliminated hyperphosphorylation, suggesting that copper binding at

282 ion of amyloid-beta oligomers as well as tau hyperphosphorylation, synapse loss, and microglial activ

283 ased amyloid-beta oligomer accumulation, tau hyperphosphorylation, synapse loss, and microglial activ

284 also reduced tau oligomer accumulation, tau hyperphosphorylation, synapse loss, and microglial activ

285 GSK-3beta was positively correlated with tau hyperphosphorylation, tangles score and Braak stage in h

286 ative diseases characterized by abnormal tau hyperphosphorylation that leads to formation of neurofib

287 patient cortical tubers were used to uncover hyperphosphorylation unique to TSC primary astrocytes, t

288 ibrate treatment significantly decreased tau hyperphosphorylation using AT8 staining and the number o

289 Disruption of BRD4 hyperphosphorylation using both chemical and molecular i

290 Notably, IFN-gamma-induced tau hyperphosphorylation was associated with release of the

291 MCV sT-associated 4E-BP1 serine 65 hyperphosphorylation was resistant to mTOR complex (mTOR

292 phosphorylation of STEP61 at multiple sites (hyperphosphorylation) was induced by the up-regulation o

293 nduced AMPK(Ser-485), but not AMPK(Thr-172), hyperphosphorylation whereas AICAR-induced Tau dephospho

294 high levels of RNA binding and disregulated hyperphosphorylation, whereas wild-type UPF1 releases fr

295 g in turn promotes ryanodine receptor type 2 hyperphosphorylation, which contributes to arrhythmogene

296 inhibiting late-acting factors triggers UPF1 hyperphosphorylation, which in turn enhances affinity fo

297 Accordingly, BAD hyperphosphorylation, which inhibits its proapoptotic ac

298 We found that OA induced in vitro tau hyperphosphorylation, which was prevented by E2 in a dos

299 erived from hTauCx3cr1(-/-) mice induces tau hyperphosphorylation within the brains of non-transgenic

300 within the eukaryotic protein kinase family, hyperphosphorylation within the kinase activation T-loop