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   2 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this
  
  
  
     6 ignalling pathway or dual inhibition (2i) of glycogen synthase kinase 3 (Gsk3) and mitogen-activated 
  
     8 cells due to its constant phosphorylation by glycogen synthase kinase 3 (GSK3) and subsequent proteas
  
  
    11 ition of protein kinase C-beta (PKCbeta) and glycogen synthase kinase 3 (GSK3) causes synergistic apo
    12 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona
  
  
  
  
  
  
  
  
    21 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui
  
  
  
    25 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm
    26 lt gastric epithelium via deletion of either glycogen synthase kinase 3 (GSK3) or APC or via expressi
  
  
  
  
    31 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain
  
  
    34  clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon
  
  
  
  
  
  
  
    42    We show that this process is dependent on glycogen synthase kinase 3 (GSK3): GSK3 was associated w
    43 : it increases Akt phosphorylation, inhibits glycogen synthase kinase 3 activity, reduces IkappaB pho
    44 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o
  
    46 evealed increased phosphorylation of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the 
  
  
  
  
    51    We identify an interaction of BMP and Wnt/glycogen synthase kinase 3 beta (GSK3beta) pathways via 
    52 dulate the activity of Tankyrase enzymes and glycogen synthase kinase 3 beta (GSK3beta), additional t
    53  activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f
    54 on on Ser(552), a site that differs from the glycogen synthase kinase 3 beta phosphorylation site.   
    55 ibition of the pro-apoptotic molecules, JNK, glycogen synthase kinase 3 beta, or caspases, toxicity i
    56 evealed a role for heat shock protein 90 and glycogen synthase kinase 3 but not casein kinase 1 nor L
    57 blocked cardiomyocyte specification, whereas glycogen synthase kinase 3 inhibition at this point enha
  
    59 thermore, sequential treatment of hPSCs with glycogen synthase kinase 3 inhibitors followed by induci
  
    61 way seems to occur from Dishevelleds to axin/glycogen synthase kinase 3(GSK3)/beta-catenin complexes 
    62 an be phosphorylated and stabilized by GSK3 (GLYCOGEN SYNTHASE KINASE 3)-like kinase BIN2 (BRASSINOST
    63 (+) NPCs with a pharmacological inhibitor of glycogen synthase kinase 3, a known regulator of WNT sig
    64 in sensitivity likely through increased Akt, glycogen synthase kinase 3, and AMPK phosphorylation; an
    65 in kinase and the Akt-mediated inhibition of glycogen synthase kinase 3, critical inhibitors of Smad 
    66  inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific
    67 y treating SH-SY5Y cells with inhibitors for glycogen synthase kinase 3-beta (GSK3beta) and cyclin-de
  
    69 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.    
  
    71 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas
  
  
  
  
  
  
  
  
  
  
  
    83 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e
  
    85  together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its i
  
    87 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap
  
    89 ositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3) and mammalian target o
    90 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin
  
    92 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p
  
  
  
    96 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru
  
  
    99 gated the effect of inhibitors targeting the glycogen synthase kinase-3 (GSK3) on the expression of N
  
  
   102 rrent study, we tested whether inhibitors of glycogen synthase kinase-3 (GSK3), previously reported t
  
   104 lian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein 
   105 ardiomyocytes in early developmental stages, glycogen synthase kinase-3 and p38 mitogen-activated pro
   106 (G6P) and reversible phosphorylation through glycogen synthase kinase-3 and the glycogen-associated f
  
   108 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi
   109  phosphorylated by recombinant GSK3beta; and glycogen synthase kinase-3 inhibitors effectively reduce
  
   111  enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)
  
  
   114 , while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signalin
   115 lations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase 
   116 ed 4 chemical compound groups: inhibitors of glycogen synthase kinase-3, p38 mitogen-activated protei
   117  to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun, 
   118 hium chloride, a reversible inhibitor of the glycogen synthase kinase-3, that rescued NMJ defects in 
  
   120  E-cadherin, and CD44-mediated signaling and glycogen synthase kinase-3/adenomatous polyposis coli-me
  
   122 y phosphorylated at Thr(714) and Ser(727) by glycogen synthase kinase 3alpha and -beta (GSK-3alpha/be
   123 m of this study was to determine the role of glycogen synthase kinase-3alpha (GSK-3alpha) in post-MI 
  
   125 ed by application of a specific inhibitor of glycogen synthase kinase 3beta (6-bromoindirubin-3'-oxim
   126 eta-catenin signaling cascades, which switch glycogen synthase kinase 3beta (GSK-3beta) activation on
  
  
  
  
   131 ected T cells and reduces phosphorylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream
   132  of cyclin B1, cyclin D3, and phosphorylated glycogen synthase kinase 3beta (GSK-3beta), while infect
  
  
   135 Akt/mammalian target of rapamycin (mTOR) and glycogen synthase kinase 3beta (GSK-3beta)/adenomatous p
   136   Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r
   137  the c-Jun N-terminal kinase (JNK)-dependent glycogen synthase kinase 3beta (GSK3beta) activity on do
   138 , N-methyl-d-aspartate receptor function, or glycogen synthase kinase 3beta (GSK3beta) activity or ex
   139 ver, hypoinsulinemia leads to an increase in glycogen synthase kinase 3beta (GSK3beta) activity that,
   140 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti
   141  (NF-kappaB) pathway and in the induction of glycogen synthase kinase 3beta (GSK3beta) activity, resu
   142 of beta-catenin by enhancing binding between glycogen synthase kinase 3beta (GSK3beta) and beta-caten
   143 tcome on different molecular targets such as glycogen synthase kinase 3beta (GSK3beta) and Forkhead b
  
   145     Unexpectedly, RNAi-mediated silencing of glycogen synthase kinase 3beta (GSK3beta) and phosphoino
   146 oteasomal degradation via phosphorylation by glycogen synthase kinase 3beta (GSK3beta) and recognitio
   147 ted protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3beta (GSK3beta) and thereby de
   148  (APC), casein kinase 1alpha (CK1alpha), and glycogen synthase kinase 3beta (GSK3beta) and undergoes 
  
   150 TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3beta) at residue K15
   151 tein, HSC70) and causes dephosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser 9 by re
   152 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s
  
   154 quent signaling, causing overt activation of glycogen synthase kinase 3beta (GSK3beta) in nerves of m
   155 synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells
  
  
  
  
  
  
  
   163 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
   164 ar carcinoma-derived KLF6 mutations affect a glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
  
  
   167 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path
  
   169 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l
   170 kt, mammalian target of rapamycin complex 1, glycogen synthase kinase 3beta (GSK3beta), and CREB.    
   171 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major 
  
   173 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p
   174 kt pathway, leading to the downregulation of glycogen synthase kinase 3beta (GSK3beta), in wild type 
  
   176 hic signaling intermediates, such as Akt and glycogen synthase kinase 3beta (GSK3beta), were dephosph
   177 y sites in the N-terminus of beta-catenin as glycogen synthase kinase 3beta (GSK3beta), which are rec
   178 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi
  
   180 1 interacts with Nrf2 and stabilizes it from glycogen synthase kinase 3beta (GSK3beta)-mediated phosp
   181 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k
  
  
  
  
  
  
  
   189 atty acids, and this suppression depended on glycogen synthase kinase 3beta activation and induction 
  
   191 au phosphorylation and solubility, increased glycogen synthase kinase 3beta activity, compromised lon
   192 protein that plays a key role in attenuating glycogen synthase kinase 3beta activity, leading to aber
   193  2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin
  
   195 isms involved demonstrate that ASPH binds to glycogen synthase kinase 3beta and inhibits its subseque
   196 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i
   197 reasing Ser9 phosphorylation-inactivation of glycogen synthase kinase 3beta by RBMY, thereby impeding
   198 of stable MT subsets through inactivation of glycogen synthase kinase 3beta by the viral Ser/Thr kina
   199 ted with release of the inhibitory effect of glycogen synthase kinase 3beta function by decreasing Se
   200 in, and that beta-catenin activation through glycogen synthase kinase 3beta inhibition leads to FANCC
   201  decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3beta levels may account for im
  
   203 in endothelial cells as reflected in Akt and glycogen synthase kinase 3beta phosphorylation, Ras-rela
  
   205 te-mediated phosphoinositide 3-kinase (PI3K)/glycogen synthase kinase 3beta signaling and decreased a
  
   207  increase in phospho-beta-catenin and active glycogen synthase kinase 3beta, a kinase known to target
   208 t3a (the canonical activator), inhibitors of glycogen synthase kinase 3beta, and small-interfering RN
   209 Akt murine thymoma viral oncogene homolog-1, glycogen synthase kinase 3beta, cyclin-dependent kinase 
  
   211 ver, inhibition of protein phosphatase 1 and glycogen synthase kinase 3beta, downstream targets of Ca
   212 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression 
  
   214 hosphorylation, downstream phosphosubstrates glycogen synthase kinase 3beta, mammalian target of rapa
   215 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o
   216 e kinase 3beta by RBMY, thereby impeding the glycogen synthase kinase 3beta-dependent degradation of 
  
  
  
  
   221 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0
  
   223 rexpression of TDP-43 leads to activation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-
   224 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking 
  
   226 etin, reactivation of beta-catenin using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiC
  
  
  
   230 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could 
   231 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa
   232  demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati
  
  
  
  
  
   238 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and 
   239  finding is the pronounced downregulation of glycogen synthase kinase-3beta (Gsk3beta) and upregulati
  
   241    Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium 
  
  
   244 uclear Nrf2 export/degradation machinery via glycogen synthase kinase-3beta (Gsk3beta) signaling was 
   245 at PAD4 recognizes, binds, and citrullinates glycogen synthase kinase-3beta (GSK3beta), both in vitro
   246 lted in increased phosphorylation of Akt and glycogen synthase kinase-3beta (GSK3beta), leading to en
  
   248 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat
   249 sed p38 mitogen-activated protein kinase and glycogen synthase kinase-3beta activity, which are belie
   250 panied by hyperphosphorylation of substrates glycogen synthase kinase-3beta and mammalian target of r
   251 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa 
   252 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa 
  
   254   Overexpression of Snail1 and inhibition of glycogen synthase kinase-3beta in colorectal tumor cells
  
   256 -beta stimulation of human keratinocytes, by glycogen synthase kinase-3beta inhibition in several epi
   257 erentiated hPSCs into mesoderm cells using a glycogen synthase kinase-3beta inhibitor for 3 days, the
   258 mbinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3beta inhibitor) caused a dose-
  
   260 ha/wrd pathway in the motoneuron antagonizes glycogen synthase kinase-3beta kinase activity to preven
   261 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re
   262      The phosphorylation and inactivation of glycogen synthase kinase-3beta was dependent on mammalia
  
   264 orylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase inv
   265 ollowed by phosphorylation (inactivation) of glycogen synthase kinase-3beta, at least in part via STA
   266  cyclin D1, E-cadherin, beta-catenin, Dvl-1, glycogen synthase kinase-3beta, axin-1, and adenomatous 
   267 no changes in Ctnnb1 expression, activity of glycogen synthase kinase-3beta, known to phosphorylate a
   268  activator of beta-catenin via inhibition of glycogen synthase kinase-3beta, reversed the inhibition 
   269 on, and increased phosphorylation of Akt and glycogen synthase kinase-3beta, ultimately resulting in 
   270 d to the phosphorylation and inactivation of glycogen synthase kinase-3beta, which resulted in inhibi
   271 inding (CREB) protein levels to decreaseviaa glycogen synthase kinase-3beta-dependent mechanism.     
  
   273 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.  
  
   275  Apc participates in a complex that includes glycogen synthase kinase beta (Gsk3beta) and betacatenin
  
  
  
   279    Studies have implicated signaling through glycogen synthase kinase (GSK) 3alpha/beta in the activa
   280  work, we demonstrate that overexpression of glycogen synthase kinase (GSK) 3beta in neural precursor
  
  
  
   284 CRMP-2 and ROCK II is partially regulated by glycogen synthase kinase (GSK)-3 phosphorylation of CRMP
  
  
  
  
  
   290 eptor is modulated, here, we have found that glycogen synthase kinase (GSK)-3beta phosphorylation of 
  
  
   293 show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a het
   294      Mechanistically, Tanshinone IIA blunted glycogen synthase kinase (GSK)3beta overactivity and hyp
   295  used to deliver low doses of small molecule glycogen synthase kinase (GSK-3) antagonists that promot
   296 sly showed that the serine/threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central 
   297 exerted its positive effect by inhibition of glycogen synthase kinase (GSK3) activity and enhancement
  
  
   300 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith
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