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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,

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