ライフサイエンスコーパス: Thr

1 Thr-381 is locked into a single conformation as an acyl

2 Thr/Tyr kinase (TTK)/monopolar spindle 1 kinase (Mps-1)

3 decreased phosphorylation of threonine 1007 (Thr-1007).

4 yphosate also contains an unreported Pro-106-Thr EPSPS target-site mutation.

5 that SC variants other than WT Ile(1)-Val(2)-Thr(3) might emerge with similar ProT-activating efficie

6 revealed that four Ser/Thr residues (Ser-20, Thr-22, Thr-182, and Thr-240) were close to the active s

7 that four Ser/Thr residues (Ser-20, Thr-22, Thr-182, and Thr-240) were close to the active site, ind

8 on the P2Y(2) phosphorylation sites Ser-243, Thr-344, and Ser-356, which are involved in receptor des

9 PEG is phosphorylated on Ser(2461)/Ser(2462)/Thr(2463) by protein kinase B (PKB) in response to insul

10 62), Ser(181), Ser(269), Ser(280), Ser(291), Thr(293), Ser(299), and Ser(302) did not affect phosphat

11 for Ca(2+)/CaM binding to activated eEF-2K (Thr-348 phosphorylated) by 20-fold.

12 (Thr) residues, namely, Ser(346), Ser(351), Thr(362), and Ser(363), and proceeded with a temporal hi

13 omplex triggered by cleavage of the Lys(368)-Thr(369) (P2-P1) reactive site bond with a stoichiometry

14 osphorylated 4E-BP1 molecules lacking Thr-37/Thr-46-priming phosphorylation.

15 Single alanine substitutions for Ser-497, Thr-500, Ser-502, Ser-506, and Ser-510 reduced maximal v

16 hat Ala substitutions of Ser-561 and Ser-641/Thr-642 recapitulate the depolarizing shift in activatio

17 horylation, specifically Ser-561 and Ser-641/Thr-642 within the first intracellular loop of the chann

18 IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFN

19 As the insertion of a Thr residue potentially creates a novel phosphorylation

20 vated carbon center, linking the oxygen of a Thr side chain to the alpha-carbon of a Gln residue.

21 led that at low pH, the N (alpha)-acetylated Thr-2 makes direct and frequent "bind-and-release" conta

22 F-2K S500D) enhances the rate of activation (Thr-348 autophosphorylation) by 6-fold and lowers the EC

23 In OVCa cells, p-Akt Thr-308 was significantly inhibited by intracellular Ca(

24 and decreased levels of active phospho-AKT (Thr-450 and Ser-473) and inactive phospho-GSK3beta (Ser-

25 complete protein sequence and located an Ala/Thr difference between the two species that explained th

26 ed translation, during which untemplated Ala/Thr residues are added C terminally to stalled peptide,

27 in analogues, each containing either an allo-Thr or an allo-Ile residue.

28 Using validated allo-Thr and allo-Ile, both l-allo-ShK and d-allo-ShK polypep

29 and EPS increased AMP accumulation and AMPK Thr(172) phosphorylation, but to a lesser degree in myot

30 ects and increased AMP accumulation and AMPK Thr(172) phosphorylation, but to a lesser degree in myot

31 EPS (24 h) increased AMP, IMP, AMPK Thr(172) phosphorylation, PGC1alpha content, and insulin

32 osphorylation at threonine residue 172 (AMPK-Thr(P)(172)).

33 among GA 3-oxidases, Tyr(93), Met(106), and Thr(202), respectively, conferred GA 3-oxidase activity

34 by phosphorylating NCOA3 at Ser (S) 1062 and Thr (T) 1067.

35 sphorylation of NACA at Thr-89, Ser-151, and Thr-174.

36 r/Thr residues (Ser-20, Thr-22, Thr-182, and Thr-240) were close to the active site, indicating their

37 for DNA-PKcs phosphorylation at Ser-2056 and Thr-2609.

38 uired for Nuf phosphorylation at Ser-225 and Thr-227, matching previous in vivo-mapped phosphorylatio

39 terminus (Ser(256), Ser(261), Ser(264), and Thr(269)), of which Ser(256) is crucial and sufficient f

40 hibitory autophosphorylation (on Thr 286 and Thr 305/306, respectively, in the human alpha isoform).

41 ins, whereas phosphorylation of Ser(383) and Thr(649) complementarily stimulates FOXO1 activity.

42 fect through phosphorylation of Ser(383) and Thr(649) in FOXO1.

43 Asn-401 and Thr-381 each form hydrogen bonds with two atoms of GSH s

44 imulated Akt phosphorylation at Ser(473) and Thr(308) in skeletal muscle, concomitant with increased

45 elopmental dephosphorylation at Thr(906) and Thr(1007) We engineered mice with heterozygous phosphomi

46 KCC2 phosphorylation at Thr(906) and Thr(1007), which inhibits KCC2 activity, underwent depho

47 cleaves DHCR24 between residues Cys(91) and Thr(92) and show that this reduces the intracellular con

48 peptide, as shown during C-terminal Ala and Thr addition (CAT-tailing) in yeast.

49 pe SLN and a pair of mutants, Asn(4)-Ala and Thr(5)-Ala, which yielded gain-of-function behavior comp

50 substitutions of Asn for Ile-136 (I136N) and Thr for Ile-142 (I142T) in a subdomain previously named

51 perturbed, however, the dynamics of Lys and Thr residues, located primarily in the imperfect KTKEGV

52 The Ser and Thr kinase AKT, also known as protein kinase B (PKB), wa

53 Modification of specific Ser and Thr residues of nucleocytoplasmic proteins with O-GlcNAc

54 NHERF1 is a phosphoprotein with 40 Ser and Thr residues.

55 effect a net dehydration reaction of Ser and Thr.

56 utamyl-tRNA-dependent dehydration of Ser and Thr.

57 amino acid diversity, foremost Gly, Ser, and Thr.

58 ssociated with binding guanine in VldE (Asn, Thr, and Val) are similar in S. venezuelae OtsA (Asp, Se

59 e evidence that the N (alpha)-acetylation at Thr-2 of EsxA facilitates dissociation of the EsxA:B het

60 ulin-dependent protein kinase II (CaMKII) at Thr(17) beta-Adrenergic stimulation and PKA-dependent ph

61 he phosphorylation and activation of CtIP at Thr-847.

62 orylation of the DNA-binding domain (DBD) at Thr-38 in CAR regulates this conversion.

63 undergoes developmental dephosphorylation at Thr(906) and Thr(1007) We engineered mice with heterozyg

64 uggest that phosphorylation of EWSR1/FLI1 at Thr 79 promotes the colocalization of EWSR1/FLI1 and Aur

65 ine kinase that phosphorylates histone H3 at Thr-3 during mitosis.

66 pendent phosphorylation of retinal IMPDH1 at Thr(159)/Ser(160) in the Bateman domain that desensitize

67 Mechanistically, phosphorylation of JMJD3 at Thr-1044 by FGF21 signal-activated PKA increases its nuc

68 he catalytic phosphorylation rate of JNK3 at Thr-221 by MKK7 is two orders of magnitude faster than t

69 h PPP1CA causes dephosphorylation of NACA at Thr-89, Ser-151, and Thr-174.

70 O-GlcNAcylation of p65 at Thr-305 and Ser-319 increased CREB-binding protein (CBP)

71 h might impair the O-GlcNAcylation of p65 at Thr-305.

72 we also identified phosphorylation of p65 at Thr-308, which might impair the O-GlcNAcylation of p65 a

73 GFR2, which, in turn, phosphorylated PERK at Thr(980) Subsequently, PERK phosphorylated eIF2alpha at

74 ltaKD fragment that is not phosphorylated at Thr(507) (which accumulates in doxorubicin-treated cardi

75 o be degraded, p27 must be phosphorylated at Thr-187 to be recognized by Skp2, a component of the ubi

76 LC3B is phosphorylated at Thr-50 within the LDS by serine/threonine kinase (STK) 3

77 phospho-isoform, EB-gamma, phosphorylated at Thr-70, Ser-83, and Ser-101, bound to eIF4E during mitos

78 -dependent beta-arrestin2 phosphorylation at Thr(383), a necessary step for Erk recruitment to the re

79 quires not only canonical phosphorylation at Thr(389) by mTORC1 but also phosphorylation at Ser(424)

80 Thus, promoting PERK phosphorylation at Thr(799) to partially down-regulate PERK-eIF2alpha signa

81 KCC2 phosphorylation at Thr(906) and Thr(1007), which inhibits KCC2 activity, un

82 the absence of Cdk2, p27 phosphorylation at Thr-187 was mainly carried out by cyclin A2-Cdk1 and cyc

83 d a PP1/2A-sensitive phosphorylation site at Thr-48 in human DAT, a residue that has not been previou

84 Substitutions at Thr-2 that precluded N (alpha)-acetylation inhibited the

85 interacted with and phosphorylated UBE2S at Thr 152, enhancing its stability by inhibiting proteasom

86 d-Aza-Thr(8),Arg(10)-teixobactin exhibits 2-8-fold greater ant

87 allographic structure of N-Me-d-Gln(4),d-aza-Thr(8),Arg(10)-teixobactin reveals an amphipathic hydrog

88 ng the importance of a hydrogen bond between Thr-238 and the substrate as well as limited cofactor di

89 olymorphism substitutions of Met residues by Thr in cancer-related proteins.

90 racts both with agonist and with a conserved Thr side chain within the receptor.

91 are efficiently mischarged, no corresponding Thr-to-Ala mistranslation is detectable.

92 loop's N-terminus to the active site Ser-Cys-Thr-Sec sequence.

93 ese results expose a unique role for deltaKD-Thr(507) phosphorylation (that does not apply to full-le

94 sing two chiral centers such as dl-Ile or dl-Thr, only the epimerization of isomers with different st

95 protein kinase substrate in vitro This dual Thr-Tyr kinase activity is also observed for a eukaryoti

96 ble Ala substitutions for Ser-497 and either Thr-500, Ser-510 or Thr-513 in WT-GC-A increased the Km

97 tification of SCF-Fbxl8 as the E3 ligase for Thr-283 phosphorylated cyclin D3.

98 pletion, showing that TARS2 is necessary for Thr-dependent mTORC1 activation.

99 linked to lysine/arginine substitutions for Thr(309) in FXII (FXII-Lys/Arg309).

100 ino acid residue 17 from the N terminus from Thr to Asn by site-directed mutagenesis, making it const

101 Lys->Arg (KR) (25/26KR and 29/31KR) and Lys->Thr (KT) (25/26KT and 29/31KT).

102 a small-molecule inhibitor against the HSP90 Thr(89) residue in conjunction with existing androgen-ab

103 antigen (PSA), is also lowered in the HSP90 Thr(89) variant.

104 MPK-mediated Ser(22) phosphorylation impairs Thr(24) phosphorylation by AKT in a hierarchical manner.

105 horylation sites in the MAD1(CTD), including Thr-716, compromised MAD2 binding and the checkpoint res

106 the side chain stereochemistry of individual Thr or Ile residues on the properties of the ShK protein

107 that phosphorylation of the newly introduced Thr residue explains the functional change.

108 (iv) Thr-315 phosphorylation is independent of intracellular

109 tion enhances signaling even in CaSs lacking Thr-888, suggesting that an additional inhibitory site e

110 n of phosphorylated 4E-BP1 molecules lacking Thr-37/Thr-46-priming phosphorylation.

111 phagic p62 degradation independently of LC3B Thr-50 phosphorylation.

112 ted by NEK9-mediated phosphorylation of LC3B Thr-50.

113 All three kinases phosphorylated LC3B Thr-50 in vitro A phospho-mimicking substitution of Thr-

114 Likewise, Thr(383) phosphorylation is involved in beta-arrestin-de

115 PKCdelta is unique in that activation loop (Thr(507)) phosphorylation is not required for catalytic

116 and JR11 = Cpa-c(dCys-Aph(Hor)-dAph(Cbm)-Lys-Thr-Cys)-dTyr-NH2)) for PET imaging.

117 og JR11 (Cpa-c[d-Cys-Aph(Hor)-d-Aph(Cbm)-Lys-Thr-Cys]-d-Tyr-NH2), an antagonist with selectivity for

118 Of note, Thr(264) is in close vicinity to a structurally and func

119 Induction of Thr(799) phosphorylation with a small-molecule activator

120 Site-directed mutagenesis of Thr-48 to Ala (T48A) to prevent phosphorylation enhanced

121 tt's lymphoma correlating with a mutation of Thr-283.

122 ) mutation, implying that phosphorylation of Thr(17) by CaMKII may become crucial for 14-3-3 recruitm

123 xpected, Akt mediates the phosphorylation of Thr(799) in PERK.

124 Phosphomimetic substitution of Thr-38 with Asp increased co-immunoprecipitation of the

125 in vitro A phospho-mimicking substitution of Thr-50 impaired binding of several LIR-containing protei

126 e-dependent kinase-1 to phosphorylate AKT on Thr-308 but insufficient to activate mTOR complex 2 (mTO

127 tein kinase undergoes autophosphorylation on Thr and Tyr residues and phosphorylates a classical euka

128 ating and inhibitory autophosphorylation (on Thr 286 and Thr 305/306, respectively, in the human alph

129 s required for subsequent phosphorylation on Thr-166 of AtRIN4, an event that is necessary and suffic

130 ent therein that supplied the codons for one Thr-Ala-Ala unit from which the extant repetitive AFGP-c

131 firm that the backbone amide of at least one Thr (Thr(304)), adjacent to conserved Ser, comes close t

132 which was abolished when Thr-89, Ser-151, or Thr-174 were substituted with phosphomimetic aspartate r

133 ed that phosphorylation at either Ser(16) or Thr(17) converted PLN into a target for the phosphoadapt

134 ts for peptides phosphorylated at Ser(16) or Thr(17) with the binding groove of 14-3-3, resulting in

135 s for Ser-497 and either Thr-500, Ser-510 or Thr-513 in WT-GC-A increased the Km 23- to 70-fold but t

136 ClC-Ka that change Ser(cen) to Gly, Pro, or Thr have only minor effects on anion selectivity, wherea

137 The frequent occurrence of Ser or Thr based helical kinks in membrane proteins suggests th

138 of N-acetylgalactosamine (GalNAc) to Ser or Thr on a protein substrate.

139 -type glycans are attached to protein Ser or Thr residues via an O-linked glycosidic bond.

140 All sites were on Ser or Thr residues, but none were on Tyr.

141 2), a residue that is semi-conserved (Ser or Thr) among vertebrate OPSR and OPSG.

142 SCF-Fbxl8 poly-ubiquitylates p-Thr-283 cyclin D3 targeting it to the proteasome.

143 (iii) Activated phospho-Thr-315 cyclin H is up-regulated during HCMV replication

144 e inhibition of fibrillation for the phospho-Thr-13 hCT analog, whereas phosphorylation in the N-term

145 ns that compromise binding of phosphorylated Thr-348 to an allosteric binding pocket on the kinase do

146 we found that PIN1 binds the phosphorylated Thr(187)-Pro motif in p27 and reduces p27's interaction

147 e serine/threonine kinase AKT phosphorylates Thr(24) and Ser(256) in FOXO1 to stimulate binding of 14

148 mediated autophagy of p62 by phosphorylating Thr-50 within the LDS of LC3B.

149 otential role of MT1-MMP cytoplasmic residue Thr(567) phosphorylation in regulation of metastasis-ass

150 impact of transporter ligands on DAT residue Thr-53, a proline-directed phosphorylation site previous

151 Residues Thr-123 and Phe-382 in the catalytic domain form a latch

152 Substitution of RIN4 Thr-166 with Asp enhanced the association of AtRIN4 with

153 rulence by promoting phosphorylation of RIN4 Thr-166, which inhibits the secretion of defense compoun

154 common amino acids, including Gly, Ala, Ser, Thr, Asp, and Glu, which are relatively silent with rega

155 that the enhanced reactivity of certain Ser, Thr, and Tyr residues occurs due to higher local concent

156 oteins weakly nucleophilic side chains (Ser, Thr, and Tyr) can be modified by DEPC in addition to oth

157 we compare DEPC labeling reactivity of Ser, Thr, and Tyr residues in intact proteins with peptide fr

158 e negative regulatory region and Pro-Glu-Ser-Thr-rich domains, the same two hotspots seen in T-cell a

159 BRAFV600E is a mutant Ser-Thr protein kinase that plays a crucial role in many typ

160 , and Sialyl-Tn (Siaalpha2-6GalNAcalpha1-Ser/Thr, STn) on their surface glycoproteins, yet molecular

161 rogenitor kinase 1 (HPK1 or MAP4K1) is a Ser/Thr kinase that operates via the c-Jun N-terminal kinase

162 transcription factor WalR, mediated by a Ser/Thr kinase-phosphatase pair PrkC/PrpC, and a Histidine k

163 Polo-like kinase 4 (PLK4) is a Ser/Thr protein kinase and the master regulator of centriole

164 We show that inhibition of CaMKII, a Ser/Thr protein kinase associated with excitability, synapti

165 p38alpha is a Ser/Thr protein kinase involved in a variety of cellular pro

166 ng axis comprising the calcium-activated Ser/Thr phosphatase calcineurin (CN), and its downstream tar

167 of TGFBRs resides inside the cells, AKT Ser/Thr kinase (AKT) activation in response to insulin or ot

168 se that phosphorylates and activates AKT Ser/Thr kinase (AKT) at Ser(473) siRNA-based gene-silencing

169 We next found that the AKT Ser/Thr kinase (AKT) inhibitor MK2206 blocks the starvation-

170 utophagy-related genes, and enhanced AKT Ser/Thr kinase (AKT) phosphorylation and cell growth.

171 igh glucose (HG)-induced profibrotic AKT Ser/Thr kinase (AKT) signaling and up-regulation of extracel

172 the phosphoinositide 3-kinase (PI3K)-AKT Ser/Thr kinase (AKT)-glycogen synthase kinase 3beta (GSK3bet

173 for phosphoinositide 3-kinase (PI3K)/AKT Ser/Thr kinase (AKT)-mediated PCFU survival.

174 6) via a signaling pathway involving AKT Ser/Thr kinase (AKT)/glycogen synthase kinase 3beta (GSK3bet

175 in the recipient cells, followed by AKT Ser/Thr kinase (AKT)/NF-kappaB activation, which promotes EM

176 hear stress stimulated activation of AKT Ser/Thr kinase 1 (AKT1), leading to phosphorylation of IGPR-

177 cells suggested that WISP1 activates AKT Ser/Thr kinase and that MEK/ERK signaling pathways shift mel

178 ed signaling and enhance or diminish AKT Ser/Thr kinase or extracellular signal-regulated kinase sign

179 phosphoinositide 3-phosphate kinase, Akt Ser/Thr kinase, nitric oxide synthase 1, nitric oxide, solub

180 tumor-associated Tn antigen (alphaGalNAc-Ser/Thr) and its sialylated form, the sialyl-Tn antigen.

181 controlled by protein ubiquitination and Ser/Thr phosphorylation.

182 found that androgen exposure antagonizes Ser/Thr kinase 4 (STK4/MST1) signaling, stimulates the activ

183 Microtubule-associated Ser/Thr kinase 2 (MAST2) inhibits neurite outgrowth, and its

184 ubunit alpha (PP1A) as a NACA-associated Ser/Thr phosphatase.

185 Phosphorylation at Ser/Thr residues may regulate the functional assembly of FUS

186 ed in the translation of the ATR and ATM Ser/Thr kinases, thereby establishing SLFN11 as a novel tRNA

187 RECQ1 loss led to defective ATR Ser/Thr kinase (ATR)/checkpoint kinase 1 (ChK1) activation a

188 GLI3 phosphorylation by Ser/Thr kinases is a primary factor for their transcriptiona

189 yme family responsible for most cellular Ser/Thr dephosphorylation events.

190 (RSK1-4) is a group of highly conserved Ser/Thr kinases that act as downstream effectors of the Ras/

191 tudy, we investigated CstK (for Coxiella Ser/Thr kinase), a protein kinase identified in C. burnetii

192 Protein kinase D (PKD) is an essential Ser/Thr kinase in animals and controls a variety of diverse

193 protein kinase 1 (CDPK1) is an essential Ser/Thr kinase that controls invasion and egress by the prot

194 chanism that is widespread in eukaryotic Ser/Thr kinases.

195 in phosphatase 2 (AtSLP2) is a bona fide Ser/Thr protein phosphatase that is targeted to the mitochon

196 creates a novel phosphorylation site for Ser/Thr kinases and because Nav1.7 had been shown in Xenopus

197 ural analysis of mPDE revealed that four Ser/Thr residues (Ser-20, Thr-22, Thr-182, and Thr-240) were

198 ss truncated O-glycans, Tn (GalNAcalpha1-Ser/Thr), and Sialyl-Tn (Siaalpha2-6GalNAcalpha1-Ser/Thr, ST

199 Very little is known about how Ser/Thr protein phosphatases specifically recruit and dephos

200 at the equivalent position in ~100 human Ser/Thr kinases, a residue that we found was important not o

201 In this work, the starvation-induced Ser/Thr protein kinase ArnS (Saci_1181) which is located pro

202 ng complex inhibits receptor-interacting Ser/Thr kinase (RIPK) activation by removing Lys-63-linked p

203 , is initiated by a receptor-interacting Ser/Thr kinase 1 (RIPK1)-ceramide complex transported to the

204 osis) by activating receptor-interacting Ser/Thr kinase 3 (RIPK3), caspase-8, and the NLRP3 inflammas

205 L.p. has 5 conserved eukaryotic-like Ser/Thr effector kinases, LegK1-4 and LegK7, which are trans

206 NACA Ser/Thr-to-alanine variants displayed increased nuclear loca

207 C-terminal prior glycosylation (GalNAc-O-Ser/Thr) preferences modulated by the lectin domain.

208 termini of the Gal((13)C(6))-Tn-occupied Ser/Thr residues from immobilized peptides to yield site-con

209 inases (PLKs), a five membered family of Ser/Thr protein kinases, have long been studied for their ro

210 to six clustered O-glycans consisting of Ser/Thr-linked N-acetylgalactosamine with beta1,3-linked gal

211 n of the RAS ITD with Raf proto-oncogene Ser/Thr kinase (RAF), leading to increased phosphorylation o

212 rated that KRAS and Raf-1 proto-oncogene Ser/Thr kinase (RAF1) domains interact with these membranes

213 ibitors targeting the RAF proto-oncogene Ser/Thr protein kinase (RAF) and MAPK/ERK kinase, indicating

214 ass 3 mutations in B-Raf proto-oncogene, Ser/Thr kinase (BRAF), that result in kinase-impaired or kin

215 and activating WT C-Raf proto-oncogene, Ser/Thr kinase (CRAF).

216 omain (RBD) of the C-Raf proto-oncogene, Ser/Thr kinase (CRAF).

217 ing 2/3 (Socs2/3); Pim-1 proto-oncogene, Ser/Thr kinase (Pim1); and Fms-related tyrosine kinase 4 (Fl

218 sulin, activation of RAF proto-oncogene, Ser/Thr kinase (Raf)-mitogen-activated protein kinase (MAPK)

219 f clients, such as Raf-1 proto-oncogene, Ser/Thr kinase (RAF1), that are particularly dependent on th

220 being mediated by Raf-1 proto-oncogene, Ser/Thr kinase (RAF1).

221 neuronal signaling by catalyzing phospho-Ser/Thr dephosphorylations in diverse substrates.

222 s other PIKKs specifically phosphorylate Ser/Thr-containing motifs with a glutamine residue at positi

223 RCT domains and conserved phosphorylated Ser/Thr residues at the C-terminus of the nucleolar phosphop

224 o acids C-terminal to the phosphorylated Ser/Thr to prime a catalytically active conformation, facili

225 Ppz Ser/Thr protein phosphatases (PPases) are found only in fung

226 , as evaluated by the ability to predict Ser/Thr/Tyr phosphorylation sites in the disordered proteome

227 lNAc) monosaccharide attached to protein Ser/Thr residues, is found on most cancer yet rarely detecte

228 gle1A(6D) variant (in which six putative Ser/Thr phosphorylation sites were substituted with Asp) per

229 Me) that is specific for cancer-relevant Ser/Thr(O)-linked N-acetylgalactosamine (GalNAc) glycosylati

230 ouble mutation of nonconserved residues (Ser/Thr(296/297)) may perturb the local fold.

231 DNA damage response Ser/Thr kinases, including ataxia telangiectasia-mutated (AT

232 correlated with peptidoglycan-responsive Ser/Thr kinases for cell signaling, and the germination of r

233 d, notably by phosphorylation of several Ser/Thr residues in the N-terminal tail.

234 CPKs are composed of a dual specificity (Ser/Thr and Tyr) kinase domain tethered to a calmodulin-like

235 While it is known that Ser/Thr protein phosphatases prefer pThr over pSer, we show

236 sis for these phenomena, we compared the Ser/Thr and Tyr phosphoproteomes of murine lung epithelial c

237 The Ser/Thr kinase 90 kDa ribosomal protein S6 kinase 1 (p90RSK)

238 K)-Akt activator, was dependent upon the Ser/Thr kinase activity of Us3.

239 nd that HTT, upon phosphorylation by the Ser/Thr kinase Akt, regulates APP transport in axons but not

240 found that the catalytic activity of the Ser/Thr kinase Aurora A was inhibited by the oxidation of a

241 ch repeats, is polyphosphorylated by the Ser/Thr kinase CotH.

242 mulates the phosphorylation of Ci by the Ser/Thr kinase Fused (Fu) and that Fu-mediated phosphorylati

243 The Ser/Thr kinase PknB, which can sense cellular lipid II level

244 We identify the Ser/Thr NDR kinase Tricornered (Trc) as a Pavarotti-dependen

245 ular pH homeostasis, is regulated by the Ser/Thr phosphatase calcineurin (CN).

246 The Ser/Thr protein kinase Akt regulates essential biological pr

247 The Ser/Thr protein kinase ataxia telangiectasia mutated (ATM) p

248 The Ser/Thr protein kinase MELK (maternal embryonic leucine zipp

249 The Ser/Thr protein kinase PINK1 phosphorylates the well-folded,

250 ases (PIKKs) are large Serine/Threonine (Ser/Thr)-protein kinases central to the regulation of many f

251 addition of GlcNAc (O-GlcNAcylation) to Ser/Thr residues of proteins and thereby contributes to diab

252 O-linkage of beta-N-acetylglucosamine to Ser/Thr residues on target proteins, is increasingly recogni

253 here the involvement of eukaryotic-type Ser/Thr kinases, particularly PknA in trans-phosphorylating

254 CK2 is a ubiquitous Ser/Thr protein kinase involved in the control of various si

255 we identified a large set of upregulated Ser/Thr phosphorylations common to both viral genotypes, whi

256 d cells was dependent upon the HSV-1 Us3 Ser/Thr kinase.

257 ERK1/2-RSK signalling inhibits EPHA2 via Ser/Thr phosphorylation, whilst FGF4-ERK1/2 disrupts a core

258 r N-glycosylation have yielded the Asn-X-Ser/Thr (NXS/T) sequon and the enhanced aromatic sequons (Ph

259 ation of Akt at its primary activation site, Thr-308.

260 phosphorylation of a newly discovered site, Thr-581.

261 e effects of two UNG2 phosphorylation sites (Thr(6) and Tyr(8)) located within its PCNA-interacting m

262 , the phosphomimetic mutant EWSR1/FLI1-T79D (Thr to aspartic acid (Asp)) retained the high activity a

263 In summary, our findings indicate that Thr(264) in TRPV3 is a key ERK phosphorylation site medi

264 to induce these phenotypes, indicating that Thr 79 is critical for EWSR1/FLI1 interference with mito

265 bed by targeted mutagenesis, indicating that Thr-28, Ser-50, Arg-51, and Arg-55 are important for dis

266 Mutational analysis revealed that Thr-1007 dephosphorylation mediated the effects of NEM o

267 Results show that Thr(567) modulation influences behavior of both individu

268 The Thr allele is extremely rare in most global populations

269 only Cdk2 but Cdk1 phosphorylates p27 at the Thr-187.

270 ontacts between the carbonyl groups from the Thr-Val-Gly-Tyr-Gly signature filter sequence and the pe

271 identification of the phosphorylation of the Thr 79 of EWSR1/FLI1 as a critical residue required for

272 63 was particularly strong; each copy of the Thr allele conferred 42% lower triglycerides (beta=-0.92

273 st that post-translational regulation of the Thr(567) in the MT1-MMP cytoplasmic tail may function as

274 Substitution of the Thr(89) in HSP90 prevented its phosphorylation by PKA an

275 und that PKA-mediated phosphorylation of the Thr(89) residue in HSP90 releases AR from HSP90, enablin

276 idence that the N (alpha)-acetylation of the Thr-2 residue on EsxA, a post-translational modification

277 P2 by ESCs is accompanied by rotation of the Thr-498 side chain in the KTG motif to contact the cepha

278 Our results showed that the Thr-to-Lys mutation of residue 367 in E protein (E367) p

279 Here, we found that the Thr-to-Lys substitution at E367 is a crucial determinant

280 We found that this Thr was critical for the association of gp120 with the v

281 that the backbone amide of at least one Thr (Thr(304)), adjacent to conserved Ser, comes close to the

282 of EWSR1/FLI1-T79A, containing a threonine (Thr) to alanine (Ala) substitution at amino acid 79, fai

283 when cytoplasmic serine (Ser) and threonine (Thr) residues are mutated.

284 arboxyl-terminal serine (Ser) and threonine (Thr) residues, namely, Ser(346), Ser(351), Thr(362), and

285 ORC1 in response to variations in threonine (Thr) levels via mitochondrial threonyl-tRNA synthetase T

286 n phosphorylation of a PXTP motif threonine (Thr(349)) located within the C-terminal alpha-arrestin d

287 containing methionine (Met; M) or threonine (Thr; T), which differentially influence natural killer a

288 ine residue (Cys(290)) that lies adjacent to Thr(288), a critical phosphorylation site in the activat

289 pped a binding pocket in mVDAC1 localized to Thr(83) and Glu(73), respectively.

290 ivity in cells lacking TARS2 is resistant to Thr repletion, showing that TARS2 is necessary for Thr-d

291 by tRNA(Gln(TTG)), tRNA(Arg(CCG)), and tRNA(Thr(CGT)) These findings collectively reveal the presenc

292 he anticodon loop of Trypanosoma brucei tRNA(Thr) is methylated to 3-methylcytosine (m(3)C) as a pre-

293 critical error of L-Ala mischarged onto tRNA(Thr), which is proofread by Animalia-specific-tRNA Deacy

294 ntains in its ion transport pathway a unique Thr-Ser-Asp (TSD) motif, which is involved in the bindin

295 uciferase reporter, which was abolished when Thr-89, Ser-151, or Thr-174 were substituted with phosph

296 de chain hydroxyl forms a hydrogen bond with Thr-498.

297 sphorlyation site in CaS that in tandem with Thr-888 controls receptor activity.

298 t through a hydrogen bond and, together with Thr-35 of WW1, form a binding pocket that accommodates a

299 d the enhanced aromatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be efficiently N-g

300 c sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be efficiently N-glycosylated.