ライフサイエンスコーパス: Thr

1 Thr(26) phosphorylation leads to charge neutralization o

2 Thr-38 dephosphorylation then dissociated the DBD-LBD in

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

4 f the C-terminal tail, designated cluster 1 (Thr(347), Thr(349), and Ser(350)) and cluster 2 (Ser(357

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

6 ogen bond network including His-47, Asp-129, Thr-171, and Ser-202, all shown to be functionally impor

7 k, which involves residues Asp-222, His-143, Thr-139, His-189, and structural waters, is located at t

8 We further identified Ser-58, Ser-155, Thr-159, and Ser-280 as the main mitotic phosphorylation

9 e activation segment of NEK3, threonine 165 (Thr-165), was identified.

10 antagonist desGly-NH2 , d(CH2 )5 [D-Tyr(2) ,Thr(4) ]OVT, the ionotropic glutamate receptor antagonis

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

12 PknA-mediated phosphorylation, where Ser-20/Thr-240 influence enzyme activity and Thr-309 endorses i

13 imulatory phosphorylation of NKCC1 (Thr(203)/Thr(207)/Thr(212)), is also essential for the inhibitory

14 phosphorylation of NKCC1 (Thr(203)/Thr(207)/Thr(212)), is also essential for the inhibitory phosphor

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

16 R2A 131His/Arg (rs1801274); 2) FCGR2B 232Ile/Thr (rs1050501); 3) TNFA -1031T/C (rs1799964); and 4) TN

17 the SNP in FCGR2A 131His/Arg, FCGR2B 232Ile/Thr, TNFA -1031T/C, and TNFA -863C/A are not associated

18 ylation of ACCbeta Ser(221), TBC1D1 Ser(237)/Thr(596), and TBC1D4 Ser(704) Conversely, exercise decre

19 22)]sCT(8-32) adopts a type II turn (Gly(28)-Thr(31)), whereas CGRP and AM adopt type I turns.

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

21 h the corresponding residues from RasGRP1/3 (Thr(7), Tyr(8), Gly(19), and Leu(21), respectively) conf

22 pha1beta2gamma1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation.

23 n sites of p65 at Thr-305, Ser-319, Ser-337, Thr-352, and Ser-374.

24 The site-specific (Val(344)-Thr(345)) and rapid (seconds to minutes) NE-based RCL pr

25 rminal tail, designated cluster 1 (Thr(347), Thr(349), and Ser(350)) and cluster 2 (Ser(357)and Ser(3

26 phorylation of beta-catenin at Ser-33/Ser-37/Thr-41.

27 np(1),Dpr(3)(6-fluoro-2-naphthoate),1-Nal(4),Thr(8)]ghrelin(1-8), possessed an IC50 value of 0.11 nM

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

29 emically identified sites (Ser-487, Ser-497, Thr-500, Ser-502, Ser-506, Ser-510, and Thr-513) and one

30 due in this motif of secretin (sec), Phe(6), Thr(7), and Leu(10), and cysteines incorporated into the

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

32 essential kinase regulators of KCC3 Thr(991)/Thr(1048) phosphorylation - a key signaling event in cel

33 inhibitory phosphorylation of KCC3 (Thr(991)/Thr(1048)).

34 hich must display a Glu residue at P-3 and a Thr residue at P-2 By means of site-directed mutagenesis

35 Finally, a Thr-to-Val replacement, which eliminates the Thr Ogamma-

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

37 APP, is related to Abeta42 by an additional Thr residue at the C-terminus.

38 lication of a highly selective OXTR agonist [Thr(4),Gly(7)]-OXT to hippocampal slices resulted in an

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

40 lternative means of activating Akt via p-Akt Thr-450, p-PDK1 Ser-241, or p-IRS1 Ser-636/639.

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

42 tion and lower cell viability than their Ala/Thr counterpart following cadmium exposure.

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

44 idues, i.e. containing d-allo-Ile and d-allo-Thr along with d-amino acids and glycine.

45 The three allo-Thr or allo-Ile-containing ShK polypeptides were able to

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

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

48 The AbetaO-dependent reduction in AMPK-Thr(P)(172) levels was mediated by glutamate receptors o

49 er that Dun1 phosphorylates Dif1 Ser-104 and Thr-105 residues upon iron scarcity.

50 e that MazF-mt6 residues Asp-10, Arg-13, and Thr-36 are critical for RNase activity and likely cataly

51 phosphorylates RIN4 at Thr-21, Ser-160, and Thr-166, leading to activation of the immune receptor RP

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

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

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

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

56 rved residues (Ser-17, Ser-249, Ser-289, and Thr-233) and thereby prevented SGT1 from associating wit

57 ore specifically, the Ser(362), Ser(363) and Thr(366) residues at the carboxyl-terminal tail were pri

58 t forms occur concurrently with Ser(473) and Thr(308) phosphorylation upon acute PI3K activation and

59 vide evidence for uncoupling of Ser(473) and Thr(308) phosphorylation, as well as differential sensit

60 497, Thr-500, Ser-502, Ser-506, Ser-510, and Thr-513) and one functionally identified putative site (

61 site residues reveals Asn(37), Asp(52), and Thr(68) are important for catalysis, and size exclusion

62 hibitors and assessed for AS160 Ser(588) and Thr(642) dephosphorylation.

63 fering RNA caused greater AS160 Ser(588) and Thr(642) phosphorylation concomitant with unaltered Akt

64 RecA undergoes phosphorylation at Tyr-77 and Thr-318 by a DNA damage-responsive serine threonine/tyro

65 Site-directed mutagenesis of Lys-85 and Thr-86 in helix 1 revealed that this interaction indeed

66 dition of one GalNAc unit each to Thr-87 and Thr-91 and one GalNAc unit to either Thr-99 or Thr-101,

67 Ser-20/Thr-240 influence enzyme activity and Thr-309 endorses its cell wall localization.

68 nascent chains with carboxy-terminal Ala and Thr extensions ("CAT tails").

69 talled NCs with a carboxy-terminal, Ala- and Thr-containing extension-the 'CAT tail'.

70 PP1) delayed AS160 Ser(588) (both doses) and Thr(642) (high dose only) dephosphorylation concomitant

71 eased the likelihood of N-glycosylation, and Thr is better than Ser at the i+2 position.

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

73 try of the chiral side chains of the Ile and Thr residues, i.e. containing d-allo-Ile and d-allo-Thr

74 Tat also induced [Ca(2+)]i increases and Thr-287 autophosphorylation of Ca(2+)/calmodulin-depende

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

76 O-glycosylation of Ser and Thr residues is an important process in all organisms, w

77 n all 11 GalNAc residues to selected Ser and Thr residues of the Thr-76-Lys-107 stretch of the mucin

78 anthipeptides include dehydration of Ser and Thr residues to dehydroalanine and dehydrobutyrine, a tr

79 etylglucosamine (GlcNAc) moieties to Ser and Thr residues.

80 iosynthesis was shown for Ala, Asp, Ser, and Thr at high rates and for Gly, Lys, Phe, Tyr, and Val at

81 ant that lacked 17 cytoplasmic Lys, Ser, and Thr residues was nearly insensitive to bortezomib treatm

82 identified PP1-alpha as a regulator of AS160 Thr(642) and Ser(588) dephosphorylation in skeletal musc

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

84 in and implicate a previously unexamined Asp-Thr dyad in catalysis of the cyclodehydration reaction.

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

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

87 y, we mapped O-GlcNAcylation sites of p65 at Thr-305, Ser-319, Ser-337, Thr-352, and Ser-374.

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

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

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

91 catalytic subunit Ssp2 is phosphorylated at Thr-189 by the upstream kinase Ssp1 in low-glucose condi

92 show that beta-arrestin2 phosphorylation at Thr(383) underlies beta-arrestin-dependent Erk1/2 activa

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

94 trate and is regulated by phosphorylation at Thr-101 (T101).

95 cetylcholine induced Plk1 phosphorylation at Thr-210 (an indication of Plk1 activation) in smooth mus

96 own of SLK inhibited Plk1 phosphorylation at Thr-210 and activation.

97 inhibition decreased Akt phosphorylation at Thr-308 and Ser-473 to extents similar to those of PDK1

98 ivated recombinant Akt by phosphorylation at Thr-308 in a Ca(2+)/CaM-dependent manner.

99 mycin (mTOR), phosphorylates PIPKIgamma90 at Thr-553 and Ser-555 and that S6K1-mediated PIPKIgamma90

100 resence of AvrB, RIPK phosphorylates RIN4 at Thr-21, Ser-160, and Thr-166, leading to activation of t

101 fe, and optimal phosphorylation of SAMHD1 at Thr(592) Furthermore, we observed that SAMHD1 mutants of

102 ion site, along with a low frequency site at Thr(40), using an in vitro phosphorylation assay combine

103 ins a consensus Mst1 phosphorylation site at Thr(89) We found that Mst1 can phosphorylate LPL in vitr

104 Conversion of the phosphorylation sites at Thr-70 and Ser-166 to Ala resulted in a loss of KIN10-de

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

106 3) interacts with and phosphorylates UNG2 at Thr(60) and that Thr(60) phosphorylation requires a Ser(

107 RCL cleavage, which occurred equally well at Thr(345)-Leu(346) and Asn(347)-Leu(348), was abolished b

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

109 II) and its autonomous activity generated by Thr-286 autophosphorylation.

110 nd the Met-Gln-Trp sequence of the canonical Thr-His-Trp (THW) loop known to interact with the methyl

111 oup is bound by a Ser-93-fatty acid carboxyl-Thr-61-His-266 hydrogen bond network.

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

113 We identified a conserved Thr-Arg motif that orients the sialic acid moiety and is

114 When this highly conserved Thr residue was substituted with anything other than ser

115 produced variants by replacing the conserved Thr-18 residue in the small subunit with Ser, Val, Gln,

116 uced by PKC-mediated phosphorylation of cTnI Thr-143.

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

118 PP2A(Ppp2r2d) dephosphorylated Thr-172 in rat aortic and human vascular smooth muscle c

119 d-allo-ShK protein revealed that diagnostic Thr and Ile signals were the same as for authentic d-ShK

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

121 -87 and Thr-91 and one GalNAc unit to either Thr-99 or Thr-101, forming a core glycopeptide for subse

122 inhibitor PD98059 blocked FSH-dependent ERK(Thr(202)/Tyr(204)) phosphorylation, demonstrating the re

123 atase (MKP3, DUSP6) inhibitors increased ERK(Thr(202)/Tyr(204)) phosphorylation in the absence of FSH

124 uding the critical residue Thr-207 (in Erk1)/Thr-188 (in Erk2).

125 ) Together these findings support a role for Thr-53 phosphorylation in regulation of transporter kine

126 e analogs of the urotensin II (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment

127 ed a homozygous mutation (p.622, encodes Ala>Thr) in RAD21 in patients from a consanguineous family w

128 udy the alpha137-141 fragment of hemoglobin (Thr-Ser-Lys-Tyr-Arg), a small (653Da) and hydrophilic an

129 t-translational modifications and identified Thr-552 as the phosphosite.

130 We recently identified Thr-348 and Ser-500 as two key autophosphorylation sites

131 ellular mutation of either of the identified Thr residues reduces the activation of Vgamma9Vdelta2 T

132 Finally, we identify Thr-313 as a residue that is critical for PINK1 catalyti

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

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

135 the side-chain stereochemistry of individual Thr or Ile residues.

136 rk2(R65S) efficiently autophosphorylates its Thr-188 even when dually mutated in the TEY motif.

137 identify essential kinase regulators of KCC3 Thr(991)/Thr(1048) phosphorylation - a key signaling eve

138 for the inhibitory phosphorylation of KCC3 (Thr(991)/Thr(1048)).

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

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

141 s-Cha-Gly-AFC (Ac-KKChaG-AFC) and acetyl-Lys-Thr-Cha-Gly-AFC (Ac-KTChaG-AFC).

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

143 and JR11 = Cpa-c(dCys-Aph(Hor)-dAph(Cbm)-Lys-Thr-Cys)-dTyr-NH2)), a novel radiolabeled sst receptor a

144 R11; DOTA-[Cpa-c(DCys-Aph(Hor)-DAph(Cbm)-Lys-Thr-Cys)-DTyr-NH2]) labeled with (177)Lu, (90)Y, and (11

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

146 fied a 5-aa-long sequence motif (Lys-Ser-Lys-Thr-Lys) in KRAS4b that may enable PDEdelta to bind both

147 Here, we report that MCa Thr(26) belongs to a consensus PKA phosphorylation site

148 of the Mst1 phosphorylation site by mutating Thr(89) to Ala impaired localization of LPL to the actin

149 We also show that mutating Thr(60) or Ser(64) to Ala increases the half-life of UNG

150 ingly, inhibition of phosphorylation at NEK3 Thr-165 by expression of a phospho-deficient mutant (NEK

151 modulatory role for phosphorylation at NEK3 Thr-165 in focal adhesion maturation and/or turnover to

152 Phosphorylation at NEK3 Thr-165 was found to be dependent on activation of the e

153 vitro treatment of synaptosomes with TAT-NET-Thr(30) (wild-type peptide) completely blocked cocaine-m

154 In vivo administration of TAT-NET-Thr(30) peptide but not TAT-NET-T30A (mutant peptide) co

155 ia the stimulatory phosphorylation of NKCC1 (Thr(203)/Thr(207)/Thr(212)), is also essential for the i

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

157 witch helix changes solvent accessibility of Thr-171 and Leu-174 that affects the domain interface.

158 This results in dephosphorylation of Thr-788/789 on the beta1-chain of alpha4beta1 and loss o

159 The functional effect of Thr(26) phosphorylation is partially mimicked by asparty

160 e ion binding sites, 2) the hydroxymethyl of Thr(772) rotates to stabilize bound Form(+) through wate

161 ing assays, we found that phosphorylation of Thr(6) or Tyr(8) on UNG2 can impede PCNA binding without

162 Phosphorylation of Thr-187 (T187) within the p27 IDR controls entry into S

163 Since phosphorylation of Thr-187 is required for this recruitment, p27T187A knock

164 nal to alpha4beta1 induce phosphorylation of Thr-758 on the beta2-chain, which is followed by binding

165 LOV protein ENVOY to interrogate the role of Thr(101) in recruiting water to the flavin active site w

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

167 Surprisingly, substitution of Thr-553 and Ser-555 with Ala promoted PIPKIgamma90 ubiqu

168 rylation of Akt on Ser(473) and FoxO1/O3a on Thr(24/32) in leukocytes and neutrophils.

169 d that >90% of its phosphorylation occurs on Thr-170, Ser-250, Ser-313, Ser-705, Ser-814, and Ser-818

170 horylated on Ser(312), Akt phosphorylated on Thr(308), and elevated TLR4 expression.

171 FSH-stimulated ERK phosphorylation on Thr(202)/Tyr(204) was PKA-dependent, but MEK(Ser(217)/Se

172 strate of 160 kDa (AS160) phosphorylation on Thr(642) and Ser(588) by Akt is essential for insulin's

173 d herein abolished SAMHD1 phosphorylation on Thr-592 during S and G2 phases thus interfering with DNA

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

175 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

176 r-91 and one GalNAc unit to either Thr-99 or Thr-101, forming a core glycopeptide for subsequent addi

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

178 y by their specificity for a targeted Ser or Thr phosphorylation site but also by binding to linear-p

179 initial N-acetylhexosamine residue to Ser or Thr.

180 ular cyclodehydration between a Cys, Ser, or Thr side chain and the backbone carbonyl carbon to form

181 it motions with larger amplitudes than other Thr residues due to solvent interactions.

182 of TPETH-2(CFTERD3) (where CFTERD is Cys-Phe-Thr-Glu-Arg-Asp) was developed for chymase detection.

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

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

185 The CTD comprises the repeated Tyr-Ser-Pro-Thr-Ser-Pro-Ser motif with potential epigenetic modifica

186 ease the surface stability of KCC2 or reduce Thr-1007 phosphorylation may be of use as enhancers of K

187 other unique features, such as Ser replacing Thr as the catalytic residue in certain BPH subfamilies,

188 that directly phosphorylates KCC2 at residue Thr-1007.

189 her residues, including the critical residue Thr-207 (in Erk1)/Thr-188 (in Erk2).

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

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

192 and phosphorylation of a threonine residue (Thr-172) within the activation loop of its kinase domain

193 ids did not involve the penultimate residue, Thr-947, which is known to be phosphorylated as part of

194 lated BiP to completion on a single residue, Thr(518).

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

196 ed by two phosphorylation events on residues Thr(308) and Ser(473) upon growth factor signaling, whic

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

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

199 Ser/Thr protein kinase (STK1) plays a critical role in cell

200 copy (NMR) reveals phosphorylation of 15 Ser/Thr sites.In vitrophosphorylation of Tau using rat brain

201 loop Tyr phosphorylation in more than 70 Ser/Thr kinases in multiple conditions, our results do not o

202 Hh pathway activity by phosphorylating a Ser/Thr cluster (CL-II) in the juxtamembrane region of Smo c

203 Sch9, a Ser/Thr kinase of AGC family (the cAMP-dependent PKA, cGMP-

204 25 to 344 revealed that WipB harbours a Ser/Thr phosphatase domain related to the eukaryotic phospho

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

206 The target of rapamycin (Tor) is a Ser/Thr protein kinase that regulates a range of anabolic an

207 PAGE gels reveal an abundance of Gly/Ala/Ser/Thr repeats exemplified by a prominent, previously unide

208 ation of tyrosine kinase c-Src (Src) and Ser/Thr kinase p38alpha (p38), demonstrating broad applicabi

209 years has been cancer-associated Tyr and Ser/Thr kinases, over 85% of the kinome has been identified

210 died for neurodegenerative diseases, and Ser/Thr phosphatases, which have been marginally aimed, even

211 controlled by protein ubiquitination and Ser/Thr phosphorylation.

212 inhibitors permitted elimination of both Ser/Thr and Tyr phosphatases and implicated dual specificity

213 is was distinct from that of a conserved Ser/Thr cluster in the more proximal C-terminus, which was r

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

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

216 d even a UDP-GlcNAc oxygen important for Ser/Thr glycosylation are irrelevant for proteolysis.

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

218 studies revealed that NisB glutamylates Ser/Thr side chains as part of the dehydration process.

219 In phase II, Ser/Thr dehydration (TclKL) and peptide macrocycle formation

220 ct and signaling-specific alterations in Ser/Thr phosphorylation of mammalian target of rapamycin, AK

221 and where the processing sites included Ser/Thr residues within +/- 4 residues that could represent

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

223 e 1 (Chk1), a DNA damage repair inducing Ser/Thr protein kinase that contains an N-terminal kinase do

224 promote dephosphorylation of inhibitory Ser/Thr residues on IRS1, including Ser(789).

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

226 PKA-dependent dephosphorylation of IRS1 Ser/Thr residues is a conserved mechanism by which GPCRs sig

227 rate is critical for proteolysis but not Ser/Thr glycosylation.

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

229 n phosphatase (PHLPP), a novel family of Ser/Thr protein phosphatases, plays an important role in reg

230 Phosphorylation of a cluster of Ser/Thr residues (amino acids 380-385) on the C-terminal tai

231 Phosphorylation of a cluster of Ser/Thr residues in the C-terminal cytoplasmic region of mel

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

233 the receptor variants that lacked Lys or Ser/Thr residues, and the hD4R mutant that lacked 17 cytopla

234 stoichiometric and site-specific phospho-Ser/Thr(s) in the C-terminal tail of PTEN.

235 cated N-terminally to the phosphorylated Ser/Thr residues in the substrate and by an acidic patch in

236 region C-terminal to the phosphorylated Ser/Thr residues.

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

238 g within the gene encoding the only PP2C Ser/Thr phosphatase in Streptococcus pneumoniae, indicating

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

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

241 ntrolled via phosphorylation at specific Ser/Thr sites.

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

243 s not only alphaGalNAc but also terminal Ser/Thr O-linked alphaGalNAc (Tn antigen).

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

245 rylation based on the maintenance of the Ser/Thr phosphatase activity and their neuroprotection again

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

247 Somatic missense mutations in the Ser/Thr protein phosphatase 2A (PP2A) Aalpha scaffold subuni

248 B of Streptococcus gordonii modifies the Ser/Thr-rich repeats of adhesin.

249 tions in 2 subunits of serine/threonine (Ser/Thr) protein phosphatase 2A (PP2A) were identified in 16

250 GlcNAc addition to serine and threonine (Ser/Thr) residues and OGA for its removal.

251 that AAL binds O-linked fucose added to Ser/Thr residues present in or adjacent to Ser-rich domains

252 terference of endogenous eukaryotic-type Ser/Thr kinases could be excluded.

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

254 y GtfA to bind substrate with unmodified Ser/Thr residues.

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

256 s examined in this study harbored the single Thr-86-Ile mutation in GyrA, FQ(R) C. jejuni isolates ha

257 un1 kinase activity and phosphorylation site Thr-380 in the Dun1 activation loop, but not the Dun1 fo

258 AMPK phosphorylation at its activating site, Thr-172.

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

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

261 mutation, which was incapable of stimulating Thr(286) autophosphorylation.

262 insulin-stimulated phosphorylation of TBC1D4 Thr(649) and Ser(711) Such findings are also evident in

263 y domain is catalytically competent and that Thr(507) phosphorylation is not required for deltaKD act

264 and phosphorylates UNG2 at Thr(60) and that Thr(60) phosphorylation requires a Ser(64) priming phosp

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

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

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

268 We show that Thr(507)-phosphorylated deltaKD is catalytically active

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

270 Our findings show that Thr-53 phosphorylation is stimulated in a transporter-de

271 The Thr allele is extremely rare in most global populations

272 The Thr(350) and Ser(349) are not necessary for ss-arrestin

273 Thr-to-Val replacement, which eliminates the Thr Ogamma-H...Ndelta1 His H-bond and decreases protein

274 63 was particularly strong; each copy of the Thr allele conferred 42% lower triglycerides (beta=-0.92

275 ysis of T101I indicates a direct role of the Thr(101) position in mediating adaptation to osmotic str

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

277 owed that the nucleophilic side chain of the Thr-192 residue at +1 of the cleavage site is required f

278 dues to selected Ser and Thr residues of the Thr-76-Lys-107 stretch of the mucin domain.

279 hylene glycol) methyl ether (aaPEG) onto the Thr residue of colistin.

280 d other mutations in GyrA in addition to the Thr-86-Ile change.

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

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

283 with either an alanine (Ala) or a threonine (Thr) at residue 391.

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

285 g that deltaKD activity is regulated through Thr(507) phosphorylation.

286 Thus, Thr can substitute for Ser for the enzymatic activities

287 al part of this alpha-helix, from Phe(93) to Thr(98), is required for binding VEGFR-3 but not VEGFR-2

288 Furthermore, alterations to Thr-104, a conserved phosphorylation site in NPF6.6, res

289 chronous addition of one GalNAc unit each to Thr-87 and Thr-91 and one GalNAc unit to either Thr-99 o

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

291 ed glycans were attached to a Ser and one to Thr.

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

293 rly hypoxia increases wobble cmo(5)U in tRNA(Thr(UGU)), which parallels translation of transcripts en

294 ding of the enlarged anticodon loop of tRNA1(Thr).

295 , aminoacylates two isoacceptor tRNAs, tRNA1(Thr) and tRNA2(Thr), that harbor anticodon loops of diff

296 two isoacceptor tRNAs, tRNA1(Thr) and tRNA2(Thr), that harbor anticodon loops of different size and

297 of MST1 in complex with the canonical tRNA2(Thr) and non-hydrolyzable analog of threonyl adenylate.

298 Intriguingly, p66 with Thr(206) and Ser(213) mutated to glutamic acid showed 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.