ライフサイエンスコーパス: Ser

1 Ser-32 has been identified as the active site in Prdx6 f

2 Ser-357 was phosphorylated in vitro by multiple kinases,

3 Ser-500 is found to undergo autophosphorylation in cells

4 Ser/Thr protein kinase (STK1) plays a critical role in c

5 Moreover, the N-terminal Ala-1-Ser-30 region of cE5 (which includes an RGD tripeptide)

6 ted SGT1 at four conserved residues (Ser-17, Ser-249, Ser-289, and Thr-233) and thereby prevented SGT

7 of the non-phosphorylated state(2.12%); (2) Ser-124 and Ser-264 become less flexible in the phosphor

8 Tyr(204) was PKA-dependent, but MEK(Ser(217)/Ser(221)) phosphorylation was not regulated; rather, MEK

9 at four conserved residues (Ser-17, Ser-249, Ser-289, and Thr-233) and thereby prevented SGT1 from as

10 sites within the AQP2 C terminus (Ser(256), Ser(261), Ser(264), and Thr(269)), of which Ser(256) is

11 hin the AQP2 C terminus (Ser(256), Ser(261), Ser(264), and Thr(269)), of which Ser(256) is crucial an

12 argeted mutagenesis, indicating that Thr-28, Ser-50, Arg-51, and Arg-55 are important for discriminat

13 ped O-GlcNAcylation sites of p65 at Thr-305, Ser-319, Ser-337, Thr-352, and Ser-374.

14 NAcylation sites of p65 at Thr-305, Ser-319, Ser-337, Thr-352, and Ser-374.

15 id transport requires URAT1 residues Cys-32, Ser-35, Phe-365 and Ile-481.

16 cetylation-phosphorylation switch at Lys-321/Ser-324 that coordinately regulates tau polymerization a

17 monstrate that serines (Ser) 346 and/or 347 (Ser-346/7) of CXCR4 are phosphorylated upon stimulation

18 Mutating SM residues Phe-35/Ser-37/Leu-65/Ile-69 into alanine, based on the key resi

19 eta1AR N-terminal O-glycosylation at Ser(37)/Ser(41) as a mechanism that prevents beta1AR N-terminal

20 lly, Neto2 was phosphorylated at serine 409 (Ser-409) by Ca(2+)/calmodulin-dependent protein kinase I

21 Seven chemically identified sites (Ser-487, Ser-497, Thr-500, Ser-502, Ser-506, Ser-510, and Thr-513

22 alanine substitutions for Ser-497, Thr-500, Ser-502, Ser-506, and Ser-510 reduced maximal velocity (

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

24 ubstitutions for Ser-497 and either Thr-500, Ser-510 or Thr-513 in WT-GC-A increased the Km 23- to 70

25 substitutions for Ser-497, Thr-500, Ser-502, Ser-506, and Ser-510 reduced maximal velocity (Vmax), wh

26 d sites (Ser-487, Ser-497, Thr-500, Ser-502, Ser-506, Ser-510, and Thr-513) and one functionally iden

27 Ser-487, Ser-497, Thr-500, Ser-502, Ser-506, Ser-510, and Thr-513) and one functionally identified pu

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

29 + 1 loop Tyr phosphorylation in more than 70 Ser/Thr kinases in multiple conditions, our results do n

30 increased the phosphorylation of serine 940 (Ser-940), whereas it decreased phosphorylation of threon

31 activation, and the SH3-GK domains exhibit a Ser-561 phosphorylation-dependent switch to a closed con

32 dues 25 to 344 revealed that WipB harbours a Ser/Thr phosphatase domain related to the eukaryotic pho

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

34 of available structural data suggests that a Ser(84)-H2O-Lys(114) hydrogen-bonding network in human s

35 The major function of O-acetyl-Ser-(thiol) lyase (OAS-TL; EC 2.5.1.47) is the formation

36 e 20 common amino acids, including Gly, Ala, Ser, Thr, Asp, and Glu, which are relatively silent with

37 c MIO prosthetic group created from (189)Ala-Ser-Gly(191) residues and the bound l-phenylalanine and

38 an proceed independently of Dapk1 or altered Ser-1303 phosphorylation.

39 In proteomic analysis, Ser-164 was identified as a major serine phosphorylation

40 phosphorylated state(2.12%); (2) Ser-124 and Ser-264 become less flexible in the phosphorylated state

41 her identified Ser-58, Ser-155, Thr-159, and Ser-280 as the main mitotic phosphorylation sites in Vgl

42 ts mimicking phosphorylation at Ser-1700 and Ser-1928 and analyzed their behavior at the membrane by

43 depending on phosphorylation on Ser-1700 and Ser-1928 at the channel C terminus.

44 ce for NMIIA phosphorylation at Ser-1916 and Ser-1943.

45 a potential kinase phosphorylating Ser-2 and Ser-5 of CTD for transcription during mitosis in the bud

46 Close proximity of Ile-207 and Ser-365 to the inserted RCL suggested that the preferred

47 to be seeded, with variants at Pro(301) and Ser(320) showing robust aggregation with seeding.

48 O-GlcNAcylation of p65 at Thr-305 and Ser-319 increased CREB-binding protein (CBP)/p300-depend

49 decreased Akt phosphorylation at Thr-308 and Ser-473 to extents similar to those of PDK1 knockdown or

50 uscle phosphorylation of TBC1D4 Ser(318) and Ser(704) and glycogen synthase activity were greater in

51 We recently identified Thr-348 and Ser-500 as two key autophosphorylation sites within eEF-

52 5 at Thr-305, Ser-319, Ser-337, Thr-352, and Ser-374.

53 orted phosphorylation events at Ser(476) and Ser(480) of Cbl-b.

54 for Ser-497, Thr-500, Ser-502, Ser-506, and Ser-510 reduced maximal velocity (Vmax), whereas glutama

55 lated phosphorylation of TBC1D4 Thr(649) and Ser(711) Such findings are also evident in prior exercis

56 n of the phosphorylation sites at Thr-70 and Ser-166 to Ala resulted in a loss of KIN10-dependent pho

57 dent phosphorylation of MLK3 on Ser(705) and Ser(758), which promotes MLK3-dependent B-Raf and ERK1/2

58 of the GluK2 C-terminal residues Ser-846 and Ser-868.

59 flammation; amyloid-beta peptide (Abeta) and Ser-202-phosphorylated Tau (p-Tau(Ser-202)) levels; and

60 d the phosphorylation of p38, ERK, CREB, and Ser-727 of STAT3 and induced nuclear translocation of pC

61 e Pi-binding residues, Ser-128 (in PiT1) and Ser-113 (in PiT2), were substituted with alanine, the Pi

62 and phosphorylates Ser-5 at the promoter and Ser-2 toward the 3' end of the gene.

63 Small residues and Ser at the i+1 position increased the likelihood of N-gl

64 30 years has been cancer-associated Tyr and Ser/Thr kinases, over 85% of the kinome has been identif

65 des controlled by protein ubiquitination and Ser/Thr phosphorylation.

66 ctively, these results indicate that the Arg/Ser encoded at the third CDR3beta residue can effectivel

67 The Arg/Ser substitution also influenced Ag recognition as deter

68 unfoldase and other unique features, such as Ser replacing Thr as the catalytic residue in certain BP

69 Cdc15 could phosphorylate Ser-5, as well as Ser-2, during transcription in mitosis is in contrast to

70 ction being achieved using a diphosphate-Asn-Ser relay.

71 Val) are similar in S. venezuelae OtsA (Asp, Ser, and Phe, respectively) but not conserved in E. coli

72 re we show that phosphorylation of PSD-95 at Ser-561 in its guanylate kinase (GK) domain, which is me

73 ndent, inhibitory phosphorylation of BTPC at Ser-451 while exhibiting: (i) a pair of Ca(2+) binding s

74 at effectively phosphorylated castor BTPC at Ser-451.

75 Phosphorylation of vertebrate cofilin at Ser-3 regulates both actin binding and severing.

76 oss of AMPK also led to dephosphorylation at Ser-555 of the known STING regulator, UNC-51-like kinase

77 ur tyrosine kinase-3 (LMTK3) and of EphA2 at Ser(897) by Akt are both necessary to promote Rab14-depe

78 viously unreported phosphorylation events at Ser(476) and Ser(480) of Cbl-b.

79 ctivated AKT directly phosphorylates FAF1 at Ser 582, which disrupts the FAF1-VCP complex and reduces

80 tifies beta1AR N-terminal O-glycosylation at Ser(37)/Ser(41) as a mechanism that prevents beta1AR N-t

81 in kinase A (PKA) phosphorylation of GRK2 at Ser-685 targets it to the plasma membrane.

82 inds to and directly phosphorylates HDAC3 at Ser-424, thereby stimulating HDAC activity.

83 DAC4), hindering phosphorylation of HDAC4 at Ser(246) and preventing its nuclear export that leads to

84 I)-associated transcription factor TIF-IA at Ser-635, precluding the assembly of transcription initia

85 Phosphorylation of IRP1 at Ser-138 increased when CIA was inhibited and was require

86 found endogenous phosphorylation of Neto2 at Ser-409 in the brain.

87 Phosphorylation of NLRC4 at Ser(533) plays a crucial role in caspase-8 activation an

88 ediated activating phosphorylation of p65 at Ser-536, contributing to NF-kappaB activation.

89 talytically active and not phosphorylated at Ser(359) in its ATP-positioning G-loop.

90 imulated expression of p53 phosphorylated at Ser-15.

91 mechanisms abrogated PKD1 phosphorylation at Ser(203), 2) siRNA-mediated knockdown of PAK1 and PAK2 i

92 ss 3T3 cells blunted PKD1 phosphorylation at Ser(203), 3) phosphorylation of Ser(203) markedly increa

93 rapid and persistent PKD1 phosphorylation at Ser(203), a highly conserved residue located within the

94 tors did not prevent PKD1 phosphorylation at Ser(203), indicating that it is not mediated by autophos

95 s proposed to involve its phosphorylation at Ser-1303 by Dapk1, that is blocked by a neuroprotective

96 ecreased levels of IQGAP1 phosphorylation at Ser-1441/1443, leading to increased binding of Rac1 to I

97 V1.2 constructs mimicking phosphorylation at Ser-1700 and Ser-1928 and analyzed their behavior at the

98 Instead, mimicking phosphorylation at Ser-1700 promoted the diffusive state of CaV1.2 irrespec

99 eover, we noted that Optn phosphorylation at Ser-177 was required for autophagosome formation but not

100 ires competence for NMIIA phosphorylation at Ser-1916 and Ser-1943.

101 is required for DNA-PKcs phosphorylation at Ser-2056 and Thr-2609.

102 s and is required for Nuf phosphorylation at Ser-225 and Thr-227, matching previous in vivo-mapped ph

103 mechanism by which Neto2 phosphorylation at Ser-409 helps restrict GluK1 targeting to the synapse.

104 STAT1 overexpression and phosphorylation at Ser-727 and Tyr-701.

105 horylation, in particular phosphorylation at Ser-845, which is crucial for AMPAR recycling and is kno

106 Conversely, loss of ERG phosphorylation at Ser-96 resulted in recruitment of EZH2 across the ERG-ci

107 ndicated that the phosphorylation of PKD1 at Ser(203) is mediated by kinases of the class I PAK subfa

108 that PAK-mediated phosphorylation of PKD1 at Ser(203) triggers its membrane dissociation and subseque

109 insulin receptor substrate (IRS) proteins at Ser sites that inhibit insulin and IGF-I signaling.

110 Phosphorylation of RCP at Ser(435) by Lemur tyrosine kinase-3 (LMTK3) and of EphA2

111 rylation of Class-2 PEPC's BTPC subunit's at Ser-451 was highly purified from COS and identified as R

112 Mechanistically, phosphorylation of SIRT1 at Ser-164 substantially inhibited its nuclear localization

113 at, in addition to inhibiting actin binding, Ser-3 modification favors formation of a cofilin-binding

114 urring activation states of PARKIN caused by Ser(65) phosphorylation (pPARKIN) and phosphorylated ubi

115 at failure to inactivate nuclear GSK3beta by Ser(389) phosphorylation causes neuronal cell death in s

116 ate that inactivation of nuclear GSK3beta by Ser(389) phosphorylation plays a key role in fear respon

117 vation via IFNbeta and IL-6 is restrained by Ser(754) phosphorylation of STAT3.

118 ytosis was distinct from that of a conserved Ser/Thr cluster in the more proximal C-terminus, which w

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

120 st one Thr (Thr(304)), adjacent to conserved Ser, comes close to the HMBPP diphosphate, whereas doubl

121 tramolecular cyclodehydration between a Cys, Ser, or Thr side chain and the backbone carbonyl carbon

122 e addition of the thiol of Cys to dehydrated Ser residues during the biosynthesis of lanthipeptides,

123 preventing phosphorylation on the downstream Ser-324 residue.

124 content and increased inhibitory PDH-E1alpha Ser(300) phosphorylation and FA oxidation.

125 After CHO, muscle PDH-E1alpha Ser(300) phosphorylation was decreased, and glucose oxid

126 l cancer therapy strategy by blocking either Ser-176 or Ser-165 phosphorylation or both of YBX1 in co

127 Endogenous Ser-561 phosphorylation is induced by synaptic NMDA rece

128 din Ser(490) and focal adhesion kinase (FAK) Ser(722) and Tyr(576).

129 rotein phosphatase 2 (AtSLP2) is a bona fide Ser/Thr protein phosphatase that is targeted to the mito

130 First, Ser(764) in ZF9 allows PRDM9c to accommodate a variable

131 morphism rs1143678 substitutes Pro(1146) for Ser in the integrin alphaM cytoplasmic tail.

132 T) GC-A, but one additional substitution for Ser-473 to make GC-A-8E resulted in the same Vmax, Km, a

133 reased Vmax Ala but not Glu substitution for Ser-497 increased the Michaelis constant (Km) approximat

134 ncreased the Km Double Ala substitutions for Ser-497 and either Thr-500, Ser-510 or Thr-513 in WT-GC-

135 Single alanine substitutions for Ser-497, Thr-500, Ser-502, Ser-506, and Ser-510 reduced

136 ructural analysis of mPDE revealed that four Ser/Thr residues (Ser-20, Thr-22, Thr-182, and Thr-240)

137 n the negative regulatory region and Pro-Glu-Ser-Thr-rich domains, the same two hotspots seen in T-ce

138 tematic mutation of tyrosine residues in Gly/Ser-Tyr-Gly/Ser motifs of the IDR reduced this effect, d

139 tion of tyrosine residues in Gly/Ser-Tyr-Gly/Ser motifs of the IDR reduced this effect, depending on

140 P-knock-out mice had less PKA activity, GRK2 Ser-685 phosphorylation, and GRK2 plasma membrane target

141 Site-directed mutagenesis revealed that GRK2 Ser-685 phosphorylation drives the association of GRK2 w

142 Using GSK3beta Ser(389) to Ala mutant mice, we show that failure to ina

143 exit, PP1-dependent dephosphorylation of Gwl Ser-883 occurs prior to dephosphorylation of other mitot

144 which mediates the dephosphorylation of Gwl Ser-883.

145 ges PP1 and Gwl association and promotes Gwl Ser-883 dephosphorylation.

146 The P domain contains an Asp-His-Ser catalytic triad that is, together with five residues

147 ound by quantitative proteomics that histone Ser-ADPr is reversible in cells during response to DNA d

148 age of the fluorogenic substrate hydrodabcyl-Ser-Phe-EDANS by the proteases thermolysin and papain.

149 s effects are negligible when a hydrophilic (Ser-109) or a hydrophobic (Ile-305) amino acid is mutate

150 We further identified Ser-58, Ser-155, Thr-159, and Ser-280 as the main mitoti

151 excitotoxicity can proceed without increased Ser-1303 phosphorylation, and is unaffected by Dapk1 def

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

153 inase 1 (Chk1), a DNA damage repair inducing Ser/Thr protein kinase that contains an N-terminal kinas

154 dings suggest that elimination of inhibitory Ser phosphorylation sites of IRS2 exerts short-term bene

155 comitant dephosphorylation of the inhibitory Ser(1105) residue in PLCbeta3.

156 the effects of mutation of five "inhibitory" Ser phosphorylation sites on IRS2 function in transgenic

157 diting complex inhibits receptor-interacting Ser/Thr kinase (RIPK) activation by removing Lys-63-link

158 via p-Akt Thr-450, p-PDK1 Ser-241, or p-IRS1 Ser-636/639.

159 umor promoter through phosphorylation of its Ser-165 residue, leading to the activation of the NF-kap

160 and S84N mutants (nearly WT efficiency for l-Ser elimination) displayed intermediate activity, all sh

161 n the other hand, the S84T (which performs l-Ser racemization activity), S84A (good kcat but high Km

162 omer pairs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral amino acids Gly, beta-Al

163 as increased IRS1 phosphorylation in liver (Ser 307) provided further evidence of insulin resistance

164 iming-site phosphorylation, increased G-loop Ser(359) phosphorylation, and defective kinase activity.

165 hD4R mutant that lacked 17 cytoplasmic Lys, Ser, and Thr residues was nearly insensitive to bortezom

166 ly, unlike in WT filamin, where PKA-mediated Ser-2152 phosphorylation is ligand-dependent, the P2204L

167 Thr(202)/Tyr(204) was PKA-dependent, but MEK(Ser(217)/Ser(221)) phosphorylation was not regulated; ra

168 Moreover, Ser(754) phosphorylation inhibits cytosolic DNA-induced

169 UNC-18 variants, created by mutating Ser(311) or Ser(322), disrupt thermotaxis and suppress P

170 we observed a substantial increase in Neto2 Ser-409 phosphorylation in the presence of CaMKII, and t

171 Moreover, Neto2 Ser-409 phosphorylation inhibited synaptic targeting of

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

173 P domain induced phosphorylation of occludin Ser(490) and focal adhesion kinase (FAK) Ser(722) and Ty

174 In vitro, autophosphorylation of Ser-500 is found to require Ca(2+) and CaM and is inhibi

175 ons of lanthipeptides include dehydration of Ser and Thr residues to dehydroalanine and dehydrobutyri

176 l death dependent on FADD but independent of Ser(533) phosphorylation.

177 death and activate caspase-8 independent of Ser(533) phosphorylation.

178 Importantly, the mutant of Ser-176 and the previously reported Ser-165 sites regula

179 at individual mutation or double mutation of Ser-1916 or Ser-1943 to alanine potently blocks recruitm

180 ocytosis, whereas phosphomimetic mutation of Ser-357 to Asp did not.

181 r, we show that a phosphomimetic mutation of Ser-561 promotes an intramolecular interaction between G

182 a cumulative inhibition of a large number of Ser- and Cys-containing enzymes participating in importa

183 The frequent occurrence of Ser or Thr based helical kinks in membrane proteins sugg

184 orylation at Ser(203), 3) phosphorylation of Ser(203) markedly increased in vitro when recombinant PK

185 eta involves Akt-mediated phosphorylation of Ser(9).

186 ed that GnRH might induce phosphorylation of Ser-10 in histone 3 (H3S10p) as part of its regulation o

187 n kinase A (PKA)-mediated phosphorylation of Ser-2152, thereby dynamically regulating the TR-actin li

188 Tau phosphorylation of Ser-324 (pSer-324) has not previously been evaluated in

189 e assembly and found that phosphorylation of Ser-324 interferes with the normal microtubule-stabilizi

190 nist, induced more robust phosphorylation of Ser-346/7 compared with CXCL12.

191 of GRK3- or PKC-mediated phosphorylation of Ser-346/7 impaired the recruitment of beta-arrestin to C

192 cularly PKCalpha, reduced phosphorylation of Ser-346/7 induced by either CXCL12 or ATI-2341.

193 K6 reduced CXCL12-induced phosphorylation of Ser-346/7 with GRK3 knockdown having the strongest effec

194 ese kinases enhanced both phosphorylation of Ser-357 and endocytosis of GPR15.

195 ow the post-translational phosphorylation of Ser-500 integrates with Ca(2+) and CaM to regulate eEF-2

196 lase that is responsible for the reversal of Ser-ADPr, we identified ARH3/ADPRHL2 as capable of effic

197 The functional role of Ser-357 in endocytosis was distinct from that of a conse

198 we show that phosphorylation of GSK3beta on Ser(389) mediated by p38 MAPK specifically inactivates n

199 ERK1/2-dependent phosphorylation of MLK3 on Ser(705) and Ser(758), which promotes MLK3-dependent B-R

200 es of CaV1.2 depending on phosphorylation on Ser-1700 and Ser-1928 at the channel C terminus.

201 moting ligand-independent phosphorylation on Ser-2152.

202 PAK1-mediated merlin phosphorylation on Ser-518 reduced merlin's interactions with both LATS1/2

203 ent mutant enhances GluA1 phosphorylation on Ser-845.

204 on of clients, such as Raf-1 proto-oncogene, Ser/Thr kinase (RAF1), that are particularly dependent o

205 idues, and hairpin-loop of three Pro and one Ser residues, as well as the absence of an N-terminal ER

206 erapy strategy by blocking either Ser-176 or Ser-165 phosphorylation or both of YBX1 in colon cancer.

207 l mutation or double mutation of Ser-1916 or Ser-1943 to alanine potently blocks recruitment of GFP-N

208 18 variants, created by mutating Ser(311) or Ser(322), disrupt thermotaxis and suppress PKC-2-depende

209 mutation of the distal C-terminal Arg-354 or Ser-357, which forms a consensus phosphorylation site fo

210 osition of Vbeta11 CDR3 can encode an Arg or Ser residue as a result of somatic rearrangement.

211 in the receptor variants that lacked Lys or Ser/Thr residues, and the hD4R mutant that lacked 17 cyt

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

213 dent kinase 9 (CDK9) recruitment and phospho-Ser 2 carboxy-terminal domain (CTD) RNA polymerase (Pol)

214 is required for stable CDK9 binding, phospho-Ser 2 RNA Pol II formation, and histone acetyltransferas

215 at BRD4 independently regulates CDK9/phospho-Ser 2 CTD RNA Pol II recruitment to the IRF3-dependent I

216 A phosphomimetic Ser-500 to aspartic acid mutation (eEF-2K S500D) enhance

217 osphorylation sites to non-phosphorylatable (Ser to Ala, SA) or phosphomimetic residues (Ser to Glu,

218 e observation that Cdc15 could phosphorylate Ser-5, as well as Ser-2, during transcription in mitosis

219 s located N-terminally to the phosphorylated Ser/Thr residues in the substrate and by an acidic patch

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

221 amino acids C-terminal to the phosphorylated Ser/Thr to prime a catalytically active conformation, fa

222 ranscription of clb2 gene and phosphorylates Ser-5 at the promoter and Ser-2 toward the 3' end of the

223 r-5 at promoter and Bur1/Ctk1 phosphorylates Ser-2 at the 3' end of the genes.

224 S, and G2), where Cdck7/Kin28 phosphorylates Ser-5 at promoter and Bur1/Ctk1 phosphorylates Ser-2 at

225 Cdc15 as a potential kinase phosphorylating Ser-2 and Ser-5 of CTD for transcription during mitosis

226 ed a down-regulation of p65 phosphorylation (Ser-536) in GIMAP6 knockdown cells, indicating that GIMA

227 ture/activity relationship study of position Ser(84), the putative re-face base.

228 es corresponding to CRS2 in CXCR4 (positions Ser-103(2.63) and Gln-301(7.39)) increased CXCL11 bindin

229 uding within the gene encoding the only PP2C Ser/Thr phosphatase in Streptococcus pneumoniae, indicat

230 of CTD by Cdc15 is independent of any prior Ser phosphorylation(s).

231 mprises the repeated Tyr-Ser-Pro-Thr-Ser-Pro-Ser motif with potential epigenetic modification sites.

232 ached to serine residues in target proteins (Ser-ADPr) and showed that this PTM is specifically made

233 PK and PI3K-AKT pathways primarily regulated Ser-727 phosphorylation, whereas a physical interaction

234 ble of efficiently and specifically removing Ser-ADPr of histones and other proteins.

235 In the conserved canonical extensin repeat, Ser-Hyp4, serine and the consecutive C4-hydroxyprolines

236 utant of Ser-176 and the previously reported Ser-165 sites regulate distinct groups of NF-kappaB targ

237 However, H443P mutant does not require Ser(533) phosphorylation for caspase-8 activation and ce

238 phosphorylation at a second serine residue, Ser-96.

239 phorylation of the GluK2 C-terminal residues Ser-846 and Ser-868.

240 sphorylated SGT1 at four conserved residues (Ser-17, Ser-249, Ser-289, and Thr-233) and thereby preve

241 as double mutation of nonconserved residues (Ser/Thr(296/297)) may perturb the local fold.

242 (Ser to Ala, SA) or phosphomimetic residues (Ser to Glu, SE) reduced Brg1 phosphorylation by CK2.

243 of mPDE revealed that four Ser/Thr residues (Ser-20, Thr-22, Thr-182, and Thr-240) were close to the

244 note, when two putative Pi-binding residues, Ser-128 (in PiT1) and Ser-113 (in PiT2), were substitute

245 Two of these residues, Ser-35 and Phe-365, are also important for urate transpo

246 Together, these studies demonstrate the role Ser-346/7 plays in arrestin recruitment and initiation o

247 D4R levels is noted when cytoplasmic serine (Ser) and threonine (Thr) residues are mutated.

248 can form Trp analogues directly from serine (Ser) and the corresponding indole analogue.

249 Here, we demonstrate that serines (Ser) 346 and/or 347 (Ser-346/7) of CXCR4 are phosphoryla

250 n of the DSL ligands Delta (Dl) and Serrate (Ser) to activate Notch signalling.

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

252 d one functionally identified putative site (Ser-473) were reported.

253 ts how phosphorylation of a regulatory site (Ser-500) integrates with Ca(2+) and CaM to influence eEF

254 discovered a distinct phosphorylation site, Ser-176, on YBX1.

255 Seven chemically identified sites (Ser-487, Ser-497, Thr-500, Ser-502, Ser-506, Ser-510, an

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

257 Upon cytosolic DNA stimulation, Ser(754) is directly phosphorylated by TBK1 in a STING-d

258 a single serine-to-asparagine substitution [Ser(139)-->Asn(139) (S139N)] in the viral polyprotein su

259 44 reduces beta-amyloid (Abeta), reduces tau Ser(396) phosphorylation, and decreases both beta-secret

260 17, and 19 post-CLP reduced Abeta and p-Tau(Ser-202) accumulation, Akt/mechanistic target of rapamyc

261 l nitric-oxide synthase, and Abeta and p-Tau(Ser-202) also increased during that time.

262 Abeta) and Ser-202-phosphorylated Tau (p-Tau(Ser-202)) levels; and RAGE, RAGE ligands, and RAGE intra

263 Skeletal muscle phosphorylation of TBC1D4 Ser(318) and Ser(704) and glycogen synthase activity wer

264 on at four sites within the AQP2 C terminus (Ser(256), Ser(261), Ser(264), and Thr(269)), of which Se

265 d serine residue near the carboxyl terminus (Ser-883 in Xenopus).

266 d of N-glycosylation, and Thr is better than Ser at the i+2 position.

267 mpared with that of WT-YBX1, confirming that Ser-176 phosphorylation is critical for the activation o

268 Our results indicate that Ser-31 phosphorylation may regulate TH subcellular local

269 We further noted that Ser-610 and Tyr-634 also contribute to the mitotic check

270 We further showed that Ser-ADPr is a major PTM in cells after DNA damage and th

271 These results suggested that Ser-357 phosphorylation critically controls the ligand-i

272 The Ser and Thr kinase AKT, also known as protein kinase B (

273 The Ser(36) is located in a loop region close to the entranc

274 The Ser/Thr protein kinase PINK1 phosphorylates the well-fol

275 functional role of TH phosphorylation at the Ser-31 site (THSer(P)-31) remains unclear.

276 nt peptide contained Ala substituted for the Ser acylation site.

277 the extracellular N terminus, including the Ser-49 residue at the location of the common S49G single

278 ibose groups onto the hydroxyl oxygen of the Ser residues of target substrates, including both PARP1

279 human serine racemase lowers the pKa of the Ser(84)re-face base.

280 We found that the Ser-96 phosphorylation resulted in dissociation of EZH2

281 (PI3K)-Akt activator, was dependent upon the Ser/Thr kinase activity of Us3.

282 Third, Ser-3 modification (i.e. substitution with Asp or phosph

283 ntly, in silico modeling validated that this Ser-to-Arg mutation could alter the structure of the CDR

284 e CTD comprises the repeated Tyr-Ser-Pro-Thr-Ser-Pro-Ser motif with potential epigenetic modification

285 ed in the tetrameric channel by a transient, Ser mediated, intrahelical hydrogen bond.

286 e interference of endogenous eukaryotic-type Ser/Thr kinases could be excluded.

287 port here the involvement of eukaryotic-type Ser/Thr kinases, particularly PknA in trans-phosphorylat

288 a of UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced after an EB; that m

289 ck one or both residues of the conserved Tyr-Ser dyad that has previously been implicated in KR-catal

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

291 ed at the 4-, 5-, 6-, and 7-positions, using Ser and readily available indole analogues as starting m

292 (ER) Ca(2+) -dependent complex with EB3 via Ser-x-Ile-Pro aminoacid motif and that disruption of STI

293 DE upon PknA-mediated phosphorylation, where Ser-20/Thr-240 influence enzyme activity and Thr-309 end

294 sity by anti-Valpha24 Abs depends on whether Ser or Arg is encoded.

295 Ser(261), Ser(264), and Thr(269)), of which Ser(256) is crucial and sufficient for AQP2 translocatio

296 otent MC4R ligands, while replacing Ala with Ser maintained MC4R potency.

297 Also, substitution of talin1 C336 with Ser enhanced the affinity of talin1, whereas substitutio

298 ng H-bond and halogen-bond interactions with Ser-876, Met-915, and Met-956.

299 s for N-glycosylation have yielded the Asn-X-Ser/Thr (NXS/T) sequon and the enhanced aromatic sequons

300 e phosphorylation, leading to subsequent YAP Ser-127 phosphorylation, YAP cytoplasmic sequestration,