ライフサイエンスコーパス: hyperphosphorylation

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

2 ension and hyperkalemia, concurrent with NCC hyperphosphorylation.

3 impairment, abnormal APP processing and tau hyperphosphorylation.

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

5 expression of PITX1 and p120RasGAP by PITX1 hyperphosphorylation.

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

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

8 oking into downstream effects leading to Tau hyperphosphorylation.

9 orylation significantly and do not represent hyperphosphorylation.

10 than viral replication via mediation of NS5A hyperphosphorylation.

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

12 cell survival, which is correlated with BAD hyperphosphorylation.

13 characterized by detergent insolubility and hyperphosphorylation.

14 ed to assess amyloid beta deposition and tau hyperphosphorylation.

15 of p107 while B55alpha knockdown results in hyperphosphorylation.

16 also inhibits Dishevelled1-induced Frizzled3 hyperphosphorylation.

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

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

19 ssociated with reactive microgliosis and tau hyperphosphorylation.

20 defects that are bypassed by reducing Rad53 hyperphosphorylation.

21 b mutually reinforce each other to induce Rb hyperphosphorylation.

22 1S-mediated tau conformation and reduced tau hyperphosphorylation.

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

24 ed CDK9 as a potential kinase mediating BRD4 hyperphosphorylation.

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

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

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

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

29 Topo I hyperphosphorylation also increases its interaction with

30 (i) viroplasm assembly correlates with NSP5 hyperphosphorylation and (ii) vNSP2 S313D colocalizes wi

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

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

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

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

35 s of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau k

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

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

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

39 These cellular changes are mediated by tau hyperphosphorylation and can be reversed through inhibit

40 Similar tau hyperphosphorylation and CCE are typical features of neu

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

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

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

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

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

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

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

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

49 nic pathway and enzymes involved both in Tau hyperphosphorylation and GR activation.

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

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

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

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

54 D mouse models suppressed AD-associated eEF2 hyperphosphorylation and improved memory deficits and hi

55 ted with worsening clinical phenotype (i.e., hyperphosphorylation and increased tauopathy spreading)

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

57 cRyr2Delta50 hearts exhibited hyperphosphorylation and inhibition of pyruvate dehydrog

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

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

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

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

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

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

64 Although tau hyperphosphorylation and neurofibrillary-like pathology

65 de) or IP(3)R-knockdown prevented the CaMKII-hyperphosphorylation and nuclear-to-cytosolic HDAC4 shif

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

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

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

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

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

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

72 d protein tau (MAPTAU) contributes to MAPTAU hyperphosphorylation and subsequent formation of neurofi

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

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

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

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

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

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

79 ng reduced Abeta accumulation as well as tau hyperphosphorylation, and improve synaptic dysfunction i

80 ligand-binding is linked to activation loop hyperphosphorylation, and indiscriminate hyperphosphoryl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Indeed, this enzyme is involved in tau hyperphosphorylation, controls a multitude of CNS-specif

99 Hyperphosphorylation correlated with increased SfIAP tur

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

101 Rb hyperphosphorylation, degradation, and binding by viral

102 y following mitogen removal that sustains Rb hyperphosphorylation, demonstrating a probabilistic rath

103 Okadaic acid induced hyperphosphorylation-dependent collapse of the keratin I

104 This hyperphosphorylation-dependent feedback mechanism may se

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

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

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

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

109 In contrast, PSC-RANTES induces CCR5 hyperphosphorylation, driving enhanced arrestin recruitm

110 hed light on the molecular mechanism of NSP5 hyperphosphorylation during infection and its involvemen

111 rmore, we investigated the mechanism of NSP5 hyperphosphorylation during RV infection using NSP5 phos

112 We recently reported CSF tau hyperphosphorylation, especially on T217, is an accurate

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

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

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

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

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

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

119 Our results argue against the hyperphosphorylation hypothesis and underscore the impor

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

121 tion and CaMKII-dependent RyR2/phospholamban hyperphosphorylation in an immortalized mouse atrial car

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

123 5b treatment reduced alphaS hyperphosphorylation in E46K-expressing human neurons, i

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

125 tophagy enhancement abolishes AD-related tau hyperphosphorylation in human neuronal cells and reverse

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

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

128 ance of revisiting the role of site-specific hyperphosphorylation in regulating tau functions in heal

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

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

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

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

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

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

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

136 Hyperphosphorylation increases the affinity of the Ana2-

137 ein acts as a scaffold and induces Frizzled3 hyperphosphorylation indirectly by recruiting other kina

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

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

140 Cyclin E-mediated Rb hyperphosphorylation induces E2F transcriptional activat

141 Our results indicate that NSP5 hyperphosphorylation is a crucial step for the assembly

142 Tau aggregation and hyperphosphorylation is a key neuropathological hallmark

143 BRD4 hyperphosphorylation is also observed in other cancers d

144 Tau hyperphosphorylation is an early step in tau-mediated ne

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

146 Hyperphosphorylation is deleterious to glycogen structur

147 Frizzled3 hyperphosphorylation is increased in Celsr3 mutant mice,

148 ossibly other tauopathies where aberrant tau hyperphosphorylation is involved.

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

150 quired for viroplasm formation and that NSP5 hyperphosphorylation is required for viroplasm assembly.

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

152 m hTau40, the truncated construct K18, and a hyperphosphorylation-mimicking mutant hTau40/3Epi.

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

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

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

156 We showed that hyperphosphorylation occurs even when ATP7B is restricte

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

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

159 Hyperphosphorylation of a serine-rich motif immediately

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

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

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

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 Finally, hyperphosphorylation of endogenous full-length Pin4 was

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

170 Further, AD-associated hyperphosphorylation of eukaryotic elongation factor 2 (

171 Signaling studies revealed hyperphosphorylation of eukaryotic translation initiatio

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

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

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

175 H (TFIIH) it activates RNA polymerase II by hyperphosphorylation of its C-terminal domain (CTD).

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

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

178 We show that hyperphosphorylation of K18 inhibits 1) its aggregation

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

180 Recent studies showed AD-associated hyperphosphorylation of mRNA translation factor eukaryot

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

182 Hyperphosphorylation of NM hTau was observed as early as

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

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

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

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

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

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

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

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

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

192 oop hyperphosphorylation, and indiscriminate hyperphosphorylation of PknB substrates as well as other

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

194 in the early stages of PstP depletion showed hyperphosphorylation of protein kinases and their substr

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

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

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

198 in nuclease activity and is characterized by hyperphosphorylation of RPA, a sensor of single-stranded

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

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

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

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

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

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

205 Hyperphosphorylation of signal transducer and activator

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

207 ivates the demethylation of histones through hyperphosphorylation of specific demethylase enzymes.

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

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

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

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

212 Hyperphosphorylation of tau and imbalanced expression of

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

214 endent kinase 5 (Cdk5) activity leads to the hyperphosphorylation of Tau and neurofilament (NF) prote

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

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

217 Pathological hyperphosphorylation of tau and subsequent aggregation t

218 We detected hyperphosphorylation of tau at multiple sites in ipsilat

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

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

221 r's disease and frontotemporal dementia, the hyperphosphorylation of tau changes its shape, binding p

222 Here we report that dietary salt induces hyperphosphorylation of tau followed by cognitive dysfun

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

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

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

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

227 Hyperphosphorylation of tau is found within dystrophic n

228 Abnormal hyperphosphorylation of tau is pivotally involved in the

229 Abnormal hyperphosphorylation of Tau leads to the formation of ne

230 s finding may be attributed to CDK5 mediated hyperphosphorylation of tau only in the female hippocamp

231 egulates beta-amyloid (Abeta) production and hyperphosphorylation of Tau protein involved in these di

232 Abnormal hyperphosphorylation of tau protein is a characteristic

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

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

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

236 Although local hyperphosphorylation of tau was increased in the dentate

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

238 dynamics, leading to elevated stability and hyperphosphorylation of tau, and eventual cognitive impa

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

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

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

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

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

244 otes the amyloidogenic processing of APP and hyperphosphorylation of tau.

245 nd AMPK pathway genes known to contribute to hyperphosphorylation of tau.

246 ing perikaryal inclusions of NF proteins and hyperphosphorylation of Tau.

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

248 at binding of Ana2 to the Sas4 G-box enables hyperphosphorylation of the Ana2 N terminus by Plk4.

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

250 AbetaOs also stimulate hyperphosphorylation of the axonal microtubule-associate

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

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

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

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

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

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

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

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

259 Hyperphosphorylation of this serine in cTnI C terminus i

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

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

262 ural protein NSP5, which undergoes a complex hyperphosphorylation process during RV infection, is req

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

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

265 To determine whether RPA2 hyperphosphorylation protects stalled forks from collaps

266 The functional significance of hyperphosphorylation remains unclear.

267 Hyperphosphorylation renders tau prone to aggregate and

268 This stress-induced hyperphosphorylation required both Cdr1 autophosphorylat

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

270 The underpinnings of STAT3 hyperphosphorylation resulting in enhanced signaling and

271 We find that CDK1/2 targets exhibit hyperphosphorylation selectively in BLBC tumors, indicat

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

273 cyclin E/A-CDK activity can only maintain Rb hyperphosphorylation starting at the onset of S phase an

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

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

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

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

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

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

280 Mutant cells exhibited Mpk1-dependent Sir3 hyperphosphorylation that contributes to subtelomeric de

281 ontributed to the emergence of a model where hyperphosphorylation triggers both tau disassociation fr

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

283 ith a high likelihood of cells sustaining Rb hyperphosphorylation until S phase, at which point cycli

284 Disruption of BRD4 hyperphosphorylation using both chemical and molecular i

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

286 In HeLa cells, stress-induced Gle1 hyperphosphorylation was dynamic, primarily in the cytop

287 Correspondingly, RBR1 hyperphosphorylation was observed in CYCA3;4 gain-of-fun

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

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

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

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

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

293 Accordingly, BAD hyperphosphorylation, which inhibits its proapoptotic ac

294 During RV infection, NSP5 undergoes hyperphosphorylation, which is primed by the phosphoryla

295 on, including elevated protein stability and hyperphosphorylation, which were associated with cogniti

296 low temperatures (2 to 6 degrees C) or upon hyperphosphorylation with Src kinase.

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

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

299 nly deacetylates tau but also suppresses tau hyperphosphorylation within the microtubule-binding regi

300 T and P301L mutant tau results in robust tau hyperphosphorylation without tangle pathology, gradually