ライフサイエンスコーパス: Ser

1 Ser deprivation resulted in ribosomal stalling on two of

2 ntified eight serine residues (i.e. Ser-114, Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Ser-748, an

3 hosphorylation of retinal IMPDH1 at Thr(159)/Ser(160) in the Bateman domain that desensitizes the enz

4 idues of the chemokine XCL1 (Val(1), Gly(2), Ser(3), and Glu(4)) contribute a large fraction of the b

5 how that SPEG is phosphorylated on Ser(2461)/Ser(2462)/Thr(2463) by protein kinase B (PKB) in respons

6 threonine (Thr) residues, namely, Ser(346), Ser(351), Thr(362), and Ser(363), and proceeded with a t

7 ynthase kinase 3 (GSK3) activity and Ser-351/Ser-356 of Nrf2.

8 ight serine residues (i.e. Ser-114, Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Ser-748, and Ser-774

9 y site in metabotropic glutamate receptor 5 (Ser-839) aligns not with CaS(T888) but instead with CaS(

10 ne residues (i.e. Ser-114, Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Ser-748, and Ser-774) as the

11 , the betaA-betaB loop Asn-55-His and Lys-57-Ser substitutions in the pS3-subunit improved carboxylat

12 Instead, we discovered four serines (Ser-59, Ser-61, Ser-83, and Ser-87) that are critical for choles

13 es (i.e. Ser-114, Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Ser-748, and Ser-774) as the target si

14 we discovered four serines (Ser-59, Ser-61, Ser-83, and Ser-87) that are critical for cholesterol-ac

15 Ser-114, Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Ser-748, and Ser-774) as the target sites of CK

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

17 isoform, EB-gamma, phosphorylated at Thr-70, Ser-83, and Ser-101, bound to eIF4E during mitosis.

18 Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Ser-748, and Ser-774) as the target sites of CKI.

19 causes dephosphorylation of NACA at Thr-89, Ser-151, and Thr-174.

20 the transcription factor WalR, mediated by a Ser/Thr kinase-phosphatase pair PrkC/PrpC, and a Histidi

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

22 AK4 inhibits ICAP1 nuclear accumulation in a Ser-10-dependent manner.

23 ble displacement bi-bi mechanism involving a Ser-His-Asp catalytic triad and unconventionally uses an

24 ic progenitor kinase 1 (HPK1 or MAP4K1) is a Ser/Thr kinase that operates via the c-Jun N-terminal ki

25 displayed enhanced innervation in mice on a Ser/Gly-free diet.

26 r, mutagenesis studies suggest that Ile-A10, Ser-A12, Leu-A13, and Glu-A17 also belong to insulin's s

27 formation of an acyl-enzyme intermediate, Ac-Ser-216, by a double displacement bi-bi mechanism involv

28 lly interacts with ABI5 at phosphoamino acid Ser-145, and reduces the phosphorylation of ABI5 and the

29 A conserved amino acid, Ser-37, is required for activity.

30 bulk of TGFBRs resides inside the cells, AKT Ser/Thr kinase (AKT) activation in response to insulin o

31 diated signaling and enhance or diminish AKT Ser/Thr kinase or extracellular signal-regulated kinase

32 of autophagy-related genes, and enhanced AKT Ser/Thr kinase (AKT) phosphorylation and cell growth.

33 HDAC6) via a signaling pathway involving AKT Ser/Thr kinase (AKT)/glycogen synthase kinase 3beta (GSK

34 ing phosphoinositide 3-phosphate kinase, Akt Ser/Thr kinase, nitric oxide synthase 1, nitric oxide, s

35 We next found that the AKT Ser/Thr kinase (AKT) inhibitor MK2206 blocks the starvat

36 lglycerol accumulation, insulin-induced Akt (Ser-473) phosphorylation, and insulin-stimulated glucose

37 Here we directly studied the role of Akt2 Ser(474) phosphorylation in 3T3-L1 adipocytes by prevent

38 nesis of a beta-arrestin binding domain (Ala-Ser-Lys) within the intracellular C terminus of 5-HT(2A)

39 rmeation pathway and buttresses the 'Gly-Ala-Ser' (GAS) constriction, thus providing a structural exp

40 f a long, defined-length, N-terminal Pro/Ala/Ser (PAS) random-coil polypeptide with IL-1Ra.

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

42 ion, whereas phosphorylation of Ser(100) and Ser(511) mediate recruitment of 14-3-3 adaptor proteins

43 acids in CsGA1ox/ds, Phe(93), Pro(106), and Ser(202), with those typically conserved among GA 3-oxid

44 rease in YAP phosphorylation at Ser(127) and Ser(397), sites targeted by LATS1/2 and with the express

45 rect interactions with residues Arg(154) and Ser(158) on the HCND.

46 eonine kinase AKT phosphorylates Thr(24) and Ser(256) in FOXO1 to stimulate binding of 14-3-3 protein

47 and its peptides indicated that Ser-285 and Ser-287 are both phosphorylated by CKII.

48 nvolved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and

49 s, namely, Ser(346), Ser(351), Thr(362), and Ser(363), and proceeded with a temporal hierarchy, with

50 15 can also be phosphorylated at Ser-448 and Ser-452 in etiolated seedlings.

51 e that facilitates recruitment of Ser-5- and Ser-2-phosphorylated RNA Pol II.

52 -targeted phosphorylation sites, Ser-502 and Ser-800, indicating involvement of PKC.

53 asing vimentin phosphorylation at Ser-55 and Ser-83 and resisting calpain digestion.

54 e show that Ala substitutions of Ser-561 and Ser-641/Thr-642 recapitulate the depolarizing shift in a

55 II phosphorylation, specifically Ser-561 and Ser-641/Thr-642 within the first intracellular loop of t

56 e protein kinases phosphorylated Ser-645 and Ser-1156 of VCS, whereas SnRK2.6 and SnRK2.10 also phosp

57 SnRK2.10 also phosphorylated VCS Ser-692 and Ser-680 of VCR.

58 nvolved in NADH binding, whereas Trp(70) and Ser(45) were the key residues for nitrobenzene binding.

59 511, Ser-602, Ser-677, Ser-705, Ser-748, and Ser-774) as the target sites of CKI.

60 gamma, phosphorylated at Thr-70, Ser-83, and Ser-101, bound to eIF4E during mitosis.

61 ed four serines (Ser-59, Ser-61, Ser-83, and Ser-87) that are critical for cholesterol-accelerated de

62 d two serine residues in TOMM34: Ser(93) and Ser(160), located in the tetratricopeptide repeat 1 (TPR

63 ycogen synthase kinase 3 (GSK3) activity and Ser-351/Ser-356 of Nrf2.

64 lso found that androgen exposure antagonizes Ser/Thr kinase 4 (STK4/MST1) signaling, stimulates the a

65 oduced prolonged activation of pro-apoptotic Ser(727) p-STAT1 and suppressed Tyr(705)-p-STAT3 for up

66 nterest to clarify in future studies how APP-Ser-675 phosphorylation promotes meprin beta-mediated AP

67 Our findings suggest that APP-Ser-675 phosphorylation alters the balance of APP proces

68 ogen bonds involving sidechains of Gln, Asn, Ser, and Tyr residues, both along and transverse to the

69 use it capitalizes on a highly conserved Asp-Ser-Leu-Asp amino acid sequence in ACPs to which acyl gr

70 at it catalyzes phosphorylation of IGPR-1 at Ser(220) The subsequent activation of IGPR-1, in turn, s

71 so increased phosphorylation of GSK-3beta at Ser(9).

72 d that SnRK1 indeed phosphorylates AtCCT1 at Ser-187, and we found that AtCCT1 phosphorylation substa

73 addition, USP52 is phosphorylated by ATM at Ser-1003 after DNA damage, which enhances the catalytic

74 tivation of RIPK1 and autophosphorylation at Ser(166) Consequently, formation of the cytosolic death-

75 Phosphodefective substitution of 4E-BP1 at Ser-83 did not change global translation or individual m

76 stance mutations also act through changes at Ser(130) and such changes drastically reduce cephalospor

77 of the mitochondrial fission factor Drp1 at Ser(616) The lack of the MCU was associated with baselin

78 bsequently, PERK phosphorylated eIF2alpha at Ser(51), upregulating its downstream effector proteins A

79 reveal that OGT O-GlcNAc-modifies eIF4G1 at Ser-61 and that this modification is critical for eIF4G1

80 GFR triggered the phosphorylation of ELK1 at Ser 383 through activating MEK/ERK signaling.

81 itutions at Ser-10, or to a lesser extent at Ser-25, within this N-terminal region inhibit ICAP1 nucl

82 nscription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic ta

83 Preventing O-GlcNAcylation at Ser-642 not only entirely precluded production of the N-

84 2 and (cardio-protective) O-GlcNAcylation at Ser-642.

85 glycogen synthase kinase 3beta (GSK3beta) at Ser-9 in the retina of WT mice but not in REDD1-deficien

86 y, we found that O-GlcNAcylation of HDAC4 at Ser-642 is cardio-protective in diabetes mellitus and co

87 d kinase 4 (PAK4) can phosphorylate ICAP1 at Ser-10 both in vitro and in cultured cells and that acti

88 GLK directly phosphorylated IQGAP1 at Ser-480 enhancing Cdc42 activation and subsequent cell m

89 otide synthesis, by phosphorylating NCOA3 at Ser (S) 1062 and Thr (T) 1067.

90 nkage and involved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK

91 re, we report that RRM1 is phosphorylated at Ser 559 by CDK2/cyclin A during S/G2 phase.

92 ular contacts for peptides phosphorylated at Ser(16) or Thr(17) with the binding groove of 14-3-3, re

93 e response, SMURF2 becomes phosphorylated at Ser(384) by ataxia telangiectasia mutated (ATM) serine/t

94 ulin stimulation, Myo1c is phosphorylated at Ser(701), leading to binding of the signaling protein 14

95 ectrometry that PTPN22 was phosphorylated at Ser(751) by PKCalpha in Jurkat and primary human T cells

96 ion of insoluble alpha-syn phosphorylated at Ser-129 (pS129-alpha-syn).

97 a2 subunit of GABA(A)Rs is phosphorylated at Ser-359 and enables dynamic regulation of GABA(A)R bindi

98 hermore, HDA15 can also be phosphorylated at Ser-448 and Ser-452 in etiolated seedlings.

99 editing, we show that Drp1 phosphorylated at Ser-637 (Drp1(pS637)) resides both in the cytosol and on

100 ins bound TET2 when it was phosphorylated at Ser-99.

101 of active c-SRC after its phosphorylation at Ser 104.

102 h a rapid decrease in YAP phosphorylation at Ser(127) and Ser(397), sites targeted by LATS1/2 and wit

103 giectasia mutated-induced phosphorylation at Ser(384) constitutes a negative feedback loop that regul

104 r, out data indicate that phosphorylation at Ser(751) mediates a reciprocal regulation of PTPN22 stab

105 induced calcium-dependent phosphorylation at Ser-41 (pGAP-43).

106 tion, decreasing vimentin phosphorylation at Ser-55 and Ser-83 and resisting calpain digestion.

107 .2 channel through direct phosphorylation at Ser-616 mediated the GSK3beta-dependent tLTP changes in

108 k of (cardio-detrimental) phosphorylation at Ser-632 and (cardio-protective) O-GlcNAcylation at Ser-6

109 rotein kinase II-mediated phosphorylation at Ser-632, pointing to a mutual posttranslational modifica

110 have been linked to GluA1 phosphorylation at Ser-845, a protein kinase A (PKA)-targeted site within i

111 d protein kinase-mediated phosphorylation at Ser-99 promotes TET2 stability and increases global DNA

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

113 LN) is targeted by protein kinase A (PKA) at Ser(16) and by Ca(2+)/calmodulin-dependent protein kinas

114 ditionally, the phosphorylation of PTPN22 at Ser(751) enhanced the interaction of PTPN22 with the car

115 The phosphorylation of PTPN22 at Ser(751) prolonged its half-life by inhibiting K48-linke

116 es, whereas a phosphomimetic substitution at Ser-331 increased the number of fragmented vacuoles.

117 t phosphorylation-mimicking substitutions at Ser-10, or to a lesser extent at Ser-25, within this N-t

118 (TBK1)-mediated phosphorylation of TRAF2 at Ser-11.

119 ta (PKCiota) directly phosphorylates UBF1 at Ser-412, thereby generating a phosphopeptide-binding epi

120 RECQ1 loss led to defective ATR Ser/Thr kinase (ATR)/checkpoint kinase 1 (ChK1) activati

121 atalytic mechanism, which we postulate to be Ser-491 and the iron-bound water/hydroxide.

122 irms the existence of a steric clash between Ser-861 and the incorporated RDV-TP.

123 GLI3 phosphorylation by Ser/Thr kinases is a primary factor for their transcript

124 ated peptide that reveals how the canonical (Ser(511)) and noncanonical (Ser(100)) 14-3-3 consensus s

125 enzyme family responsible for most cellular Ser/Thr dephosphorylation events.

126 Among them, we confirmed Ser-78 in centrosomal protein 131 (CEP131, also known as

127 ted degradation, with MS analysis confirming Ser-83 as a ubiquitination site.

128 rely on anions interacting with a conserved Ser residue (Ser(cen)) at the center of three anion bind

129 is study, we investigated CstK (for Coxiella Ser/Thr kinase), a protein kinase identified in C. burne

130 CTCF Ser(224)-P is chromatin-associated, mapping to at least

131 TLR2 signaling was induced with Pam(3)Cys-Ser-Lys(4), and the role of ERK signaling was interrogat

132 The Cys/Ser mutation does not affect NO dioxygenase activity, an

133 CycA is a critically important conduit for d-Ser uptake that is central to the niche restriction of E

134 he implication of cytoplasmic transport in d-Ser toxicity was unsurprising, disruption of a single tr

135 r activation of a previously nonfunctional d-Ser deaminase.

136 s no longer compromised in the presence of d-Ser.

137 hagic Escherichia coli (EHEC) to d-serine (d-Ser) resulted in down-regulation of type 3 secretion sys

138 we have explored the adaptation of EHEC to d-Ser and its consequences for pathogenesis.

139 ivity normally associated with exposure to d-Ser.

140 be attributed to disruption of one of two d-Ser transporters and/or activation of a previously nonfu

141 contrast, the model compound prepared with d-Ser predominantly cyclized with the (1 S,2 S)-2-aminocyc

142 mouse model with a phosphorylation-defective Ser-16 to Ala-16 substitution in AMELX.

143 A can interact with TET2 and dephosphorylate Ser-99.

144 Numerous diacylglyceryltrimethylhomo-Ser (DGTS), phosphatidylcholine (PC), monogalactosyldiac

145 etween levels of diacylglyceryltrimethylhomo-Ser (DGTS) and phosphatidylcholine (PC) lipids measured

146 We propose that these two different Ser codons independently emerged during evolution.

147 uliarly, Ser is separated into two disparate Ser codon boxes, differing by at least two-base substitu

148 637), and inhibited phosphorylation of DRP1 (Ser 616).

149 orskolin stimulated phosphorylation of DRP1 (Ser 637), and inhibited phosphorylation of DRP1 (Ser 616

150 nous Ser (exSer)-dependent PDAC cells during Ser/Gly (glycine) deprivation.

151 1, we identified eight serine residues (i.e. Ser-114, Ser-475, Ser-511, Ser-602, Ser-677, Ser-705, Se

152 demonstrated that phosphorylation at either Ser(16) or Thr(17) converted PLN into a target for the p

153 Using this approach, we target an elusive Ser 405 O-GlcNAc site on OGA, showing that this site-spe

154 ioinformatics approaches confirmed that Env7 Ser-331 is within a motif that is highly conserved in ST

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

156 arbonates and cationic oligo(serine esters), Ser-CARTs are readily prepared (one flask) by a mild rin

157 y mechanism that is widespread in eukaryotic Ser/Thr kinases.

158 ine (Ser) to support the growth of exogenous Ser (exSer)-dependent PDAC cells during Ser/Gly (glycine

159 ddition to its well-known role to facilitate Ser-122 activation.

160 o Ser codons, as some genes use only AGY for Ser in their genes.

161 MoFePs evolved with specific preferences for Ser and Tyr ligands, respectively, and that the structur

162 lly creates a novel phosphorylation site for Ser/Thr kinases and because Nav1.7 had been shown in Xen

163 , and to contain a conserved and functional Ser/His/Asp catalytic triad.

164 xpress truncated O-glycans, Tn (GalNAcalpha1-Ser/Thr), and Sialyl-Tn (Siaalpha2-6GalNAcalpha1-Ser/Thr

165 y GAZ [Z = A or G]), glycine (coded by GGX), Ser (coded by AGY), and Arg (coded by CGX and AGZ).

166 N-amino acid combinations; GlcN-Gly and GlcN-Ser were best discriminated.

167 reduced amino acid diversity, foremost Gly, Ser, and Thr.

168 C pair with FemA and FemB to incorporate Gly-Ser dipeptides into cross-bridges and to confer resistan

169 ent at the equivalent position in ~100 human Ser/Thr kinases, a residue that we found was important n

170 We initially identified Ser-359 phosphorylation by MS analysis, and additional e

171 enzyme is due to a conformational change in Ser(130), and this change also leads to decreased inhibi

172 D brain, seven different residues, including Ser-675 (APP(695) numbering) in the APP cytoplasmic doma

173 Noptosis) by activating receptor-interacting Ser/Thr kinase 3 (RIPK3), caspase-8, and the NLRP3 infla

174 gon induced AMPKalpha phosphorylation at its Ser(485/491) residue, they did not affect its activity.

175 t and demonstrated that substitutions in its Ser-His-Asp triad, proposed to serve a general acid-base

176 mational states that are the result of a key Ser(4)-Pro(5) cis-trans isomerization.

177 d by A-MWCNT/Hyalu/l-Cys and A-MWCNT/Hyalu/l-Ser modified electrodes.

178 ) and 2.6 uA/nM (Pb(II)) for A-MWCNT/Hyalu/l-Ser/GCE.

179 0.034 ug L(-1) (Pb(II)) for A-MWCNT/Hyalu/l-Ser/GCE.

180 fied with l-cysteine (l-Cys) and l-serine (l-Ser).

181 AMPK-mediated Ser(22) phosphorylation directly and indirectly averts b

182 Added phosphate blocked PP1alpha-mediated Ser(290) dephosphorylation of recombinant NHERF1.

183 w that cMLCK specifically monophosphorylates Ser(23) of human cardiac troponin I (cTnI) in isolation

184 o previous reports, we did not observe Myo1c Ser(701) phosphorylation by Ca(2+)/CaM-dependent protein

185 NACA Ser/Thr-to-alanine variants displayed increased nuclear

186 (Ser) and threonine (Thr) residues, namely, Ser(346), Ser(351), Thr(362), and Ser(363), and proceede

187 ing an MICU1 contact interface with a nearby Ser residue at the cytoplasmic entrance of the MCU pore.

188 w the canonical (Ser(511)) and noncanonical (Ser(100)) 14-3-3 consensus sites on CaMKK2 cooperate to

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

190 Moreover, we found that in the absence of Ser-11 phosphorylation, the TRAF2 RING domain interacts

191 n of Lys-43 and with the peptide backbone of Ser-328 and Gly-329 from both subunits.

192 Later in evolution, another class of Ser codons, UCX, were derived from alanine codons, GCX,

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

194 re that phosphorylation/dephosphorylation of Ser(315) in flotillin-1 significantly affects its intera

195 hat 14-3-3beta binds to Myo1c independent of Ser(701) phosphorylation in vitro Additionally, in contr

196 h CLC channels and antiporters, mutations of Ser(cen) alter the anion selectivity.

197 dulin activation, whereas phosphorylation of Ser(100) and Ser(511) mediate recruitment of 14-3-3 adap

198 ulation and PKA-dependent phosphorylation of Ser(16) acutely stimulate the sarcoplasmic reticulum cal

199 Phosphorylation of Ser(16) was disrupted by the cardiomyopathy-associated D

200 In addition, we show that phosphorylation of Ser(3) may be an additional mechanism to protect RGS2 fr

201 14-3-3 proteins, whereas phosphorylation of Ser(383) and Thr(649) complementarily stimulates FOXO1 a

202 PKA-dependent phosphorylation of Ser(495) directly impairs calcium-calmodulin activation,

203 The phosphorylation of Ser(751) did not affect the recruitment of PTPN22 R620W

204 ent of muscarinic-induced phosphorylation of Ser-239 in vasodilator-stimulated phosphoprotein.

205 e imaging, we report that phosphorylation of Ser-2808 in RyR2 induced by the muscarinic receptor agon

206 at although PLK4-mediated phosphorylation of Ser-78 is dispensable for CEP131 localization, ciliogene

207 in landscape that facilitates recruitment of Ser-5- and Ser-2-phosphorylated RNA Pol II.

208 orylation, we show that Ala substitutions of Ser-561 and Ser-641/Thr-642 recapitulate the depolarizin

209 Here we show that SPEG is phosphorylated on Ser(2461)/Ser(2462)/Thr(2463) by protein kinase B (PKB)

210 CK2alpha-dependent G3BP1 phosphorylation on Ser 149 after axotomy releases axonal mRNAs for translat

211 in upon EGF-AKT1-mediated phosphorylation on Ser(552), and promotes its ubiquitylation and degradatio

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

213 ction of the RAS ITD with Raf proto-oncogene Ser/Thr kinase (RAF), leading to increased phosphorylati

214 inhibitors targeting the RAF proto-oncogene Ser/Thr protein kinase (RAF) and MAPK/ERK kinase, indica

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

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

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

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

219 , we showed that KRAS depletion leads to p53 Ser-15 phosphorylation (P-p53) and increases the levels

220 Plk1 knockdown inhibited paxillin Ser-272 phosphorylation, centrosome maturation, and cell

221 pectedly found that phosphorylated paxillin (Ser-272) was localized in centrosomes of human smooth mu

222 Peculiarly, Ser is separated into two disparate Ser codon boxes, dif

223 ed peptide with the sequence Ser-Val-Ala-Phe-Ser (SVAFS) displayed robust blocking activity against s

224 that PP2A-B55alpha dephosphorylates phospho-Ser(315) Spreading, attachment, migration, and in vitro

225 ting post-translational modification phospho-Ser-127 in YAP1, coinciding with increased YAP1 nuclear

226 e by preventing dephosphorylation of phospho-Ser(495) We also report the crystal structure of 14-3-3z

227 or androgen's inactivating effect on phospho-Ser-127 levels and increased YAP1 nuclear entry.

228 atase 2A, and thereby attenuates the phospho-Ser-127 modification and promotes YAP1 nuclear localizat

229 uring transcriptional elongation, phosphoryl-Ser(5) (pSer(5)) is gradually dephosphorylated by CTD ph

230 rhaps other PIKKs specifically phosphorylate Ser/Thr-containing motifs with a glutamine residue at po

231 ts BRCT domains and conserved phosphorylated Ser/Thr residues at the C-terminus of the nucleolar phos

232 All three protein kinases phosphorylated Ser-645 and Ser-1156 of VCS, whereas SnRK2.6 and SnRK2.1

233 skeletal muscle, p38beta MAPK phosphorylates Ser-12 on p300 to stimulate C/EBPbeta acetylation, which

234 ls and cultured neurons, SRPK phosphorylates Ser-Arg motifs in RNF12/RLIM, a key developmental E3 ubi

235 kinase in P. falciparum that phosphorylates Ser-33 of PfCRT.

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

237 sting that NHERF1 dephosphorylation precedes Ser(290) rephosphorylation.

238 tion, as evaluated by the ability to predict Ser/Thr/Tyr phosphorylation sites in the disordered prot

239 orylation in 3T3-L1 adipocytes by preventing Ser(474) phosphorylation without perturbing mTORC2 activ

240 stinctly different from the other primordial Ser codon, AGY.

241 lipases/esterases, GDSL lipases, proteases, Ser carboxypeptidases, ABHD protein, pectin acetylestera

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

243 (GalNAc) monosaccharide attached to protein Ser/Thr residues, is found on most cancer yet rarely det

244 lNAzMe) that is specific for cancer-relevant Ser/Thr(O)-linked N-acetylgalactosamine (GalNAc) glycosy

245 Located adjacent to proton shuttle residue Ser(130), it is suggested to play a role in proton trans

246 S1 pocket, the inhibitor C-terminal residue Ser(33) cleavage, and the cyclization of ToPI1 via a pep

247 a backbone amidate and an oxygenic residue (Ser or Tyr) ligate to two of the cluster's Fe centers.

248 ns interacting with a conserved Ser residue (Ser(cen)) at the center of three anion binding sites in

249 phosphorylation at a single serine residue, Ser-177.

250 DNA damage response Ser/Thr kinases, including ataxia telangiectasia-mutated

251 not correlated with peptidoglycan-responsive Ser/Thr kinases for cell signaling, and the germination

252 l natriuretic peptide receptor-cGMP-PKG-RyR2 Ser-2808 signaling and independent of muscarinic-induced

253 An RCL-derived peptide with the sequence Ser-Val-Ala-Phe-Ser (SVAFS) displayed robust blocking ac

254 m-leucine (Leu), arginine (Arg), and serine (Ser)-are encoded by six different codons.

255 ylated peptides containing catalytic serine (Ser(148)) suggesting a selective carbamylation of the en

256 found that peripheral axons release serine (Ser) to support the growth of exogenous Ser (exSer)-depe

257 primarily at four carboxyl-terminal serine (Ser) and threonine (Thr) residues, namely, Ser(346), Ser

258 Instead, we discovered four serines (Ser-59, Ser-61, Ser-83, and Ser-87) that are critical fo

259 Dl and Serrate (Ser) function redundantly in the third division.

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

261 tion of the sole AMELX phosphorylation site (Ser-16) in vitro greatly enhances its capacity to stabil

262 ting two PKC-targeted phosphorylation sites, Ser-502 and Ser-800, indicating involvement of PKC.

263 lted in ribosomal stalling on two of the six Ser codons, TCC and TCT, and allowed the selective trans

264 idues 506-517, including the kinase-specific Ser-511 residue.

265 ites of CaMKII phosphorylation, specifically Ser-561 and Ser-641/Thr-642 within the first intracellul

266 SRF Ser(103) phosphorylation is bidirectionally regulated by

267 SRF Ser(103) phosphorylation is significantly decreased in d

268 eptidase (CGEP) is a homo-oligomeric stromal Ser-type (S9D) peptidase with both exo- and endo-peptida

269 4, leading to Pol III derepression, and that Ser 45, found only in plant MAF1 proteins, is critical f

270 tion to the Env7 C terminus and confirm that Ser-331 is a primary and preferred phosphorylation site.

271 lipin 1beta and its peptides indicated that Ser-285 and Ser-287 are both phosphorylated by CKII.

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

273 The Ser protease inhibitor AEBSF (4-[2-aminoethyl] benzene s

274 The Ser/Arg (SR)-rich splicing factor (SRSF) protein kinase

275 The Ser/Thr protein kinase MELK (maternal embryonic leucine

276 found that HTT, upon phosphorylation by the Ser/Thr kinase Akt, regulates APP transport in axons but

277 e-rich repeats, is polyphosphorylated by the Ser/Thr kinase CotH.

278 stimulates the phosphorylation of Ci by the Ser/Thr kinase Fused (Fu) and that Fu-mediated phosphory

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

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

281 we found that the catalytic activity of the Ser/Thr kinase Aurora A was inhibited by the oxidation o

282 n of 14-3-3 proteins with TET2 protected the Ser-99 phosphorylation, and disruption of this interacti

283 ld higher than WT and 2-fold higher than the Ser(838)-harboring homodimer.

284 ns in its ion transport pathway a unique Thr-Ser-Asp (TSD) motif, which is involved in the binding of

285 kinases (PIKKs) are large Serine/Threonine (Ser/Thr)-protein kinases central to the regulation of ma

286 ing O-linkage of beta-N-acetylglucosamine to Ser/Thr residues on target proteins, is increasingly rec

287 espiratory CO(2) release and impaired Gly-to-Ser turnover after a shift from high-to-low CO(2) withou

288 ally targeted two serine residues in TOMM34: Ser(93) and Ser(160), located in the tetratricopeptide r

289 sed charge-altering releasable transporters (Ser-CARTs).

290 ensive disparities in the usage of these two Ser codons, as some genes use only AGY for Ser in their

291 h a functional ECT2 BRCT domain and the UBF1 Ser-412 phosphorylation site are required for UBF1-media

292 ected cells was dependent upon the HSV-1 Us3 Ser/Thr kinase.

293 beta(1)AR-induced phosphorylation of USP20 Ser-333 by protein kinase A-alpha (PKAalpha) was require

294 SnRK2.6 and SnRK2.10 also phosphorylated VCS Ser-692 and Ser-680 of VCR.

295 GF4-ERK1/2-RSK signalling inhibits EPHA2 via Ser/Thr phosphorylation, whilst FGF4-ERK1/2 disrupts a c

296 ephosphorylated by CTD phosphatases, whereas Ser(2) phosphorylation accumulates.

297 s into the CD40 signaling mechanisms whereby Ser-11 phosphorylation controls RING domain-dependent su

298 nfirmed that HNF4alpha formed a complex with Ser 100-phosphorylated RORalpha, as shown by supershifte

299 nd proceeded with a temporal hierarchy, with Ser(346) as the first site of phosphorylation.

300 gand to the heme iron has been replaced with Ser) generated variants that selectively functionalize b