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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
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
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
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
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
34 of available structural data suggests that a Ser(84)-H2O-Lys(114) hydrogen-bonding network in human s
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
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
45 a potential kinase phosphorylating Ser-2 and Ser-5 of CTD for transcription during mitosis in the bud
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
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
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
64 30 years has been cancer-associated Tyr and Ser/Thr kinases, over 85% of the kinome has been identif
66 ctively, these results indicate that the Arg/Ser encoded at the third CDR3beta residue can effectivel
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
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
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
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
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
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
99 eover, we noted that Optn phosphorylation at Ser-177 was required for autophagosome formation but not
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.
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.
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
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,
126 l cancer therapy strategy by blocking either Ser-176 or Ser-165 phosphorylation or both of YBX1 in co
129 rotein phosphatase 2 (AtSLP2) is a bona fide Ser/Thr protein phosphatase that is targeted to the mito
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-
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
143 exit, PP1-dependent dephosphorylation of Gwl Ser-883 occurs prior to dephosphorylation of other mitot
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
151 excitotoxicity can proceed without increased Ser-1303 phosphorylation, and is unaffected by Dapk1 def
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
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
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
170 we observed a substantial increase in Neto2 Ser-409 phosphorylation in the presence of CaMKII, and t
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
175 ons of lanthipeptides include dehydration of Ser and Thr residues to dehydroalanine and dehydrobutyri
179 at individual mutation or double mutation of Ser-1916 or Ser-1943 to alanine potently blocks recruitm
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
184 orylation at Ser(203), 3) phosphorylation of Ser(203) markedly increased in vitro when recombinant PK
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
189 e assembly and found that phosphorylation of Ser-324 interferes with the normal microtubule-stabilizi
191 of GRK3- or PKC-mediated phosphorylation of Ser-346/7 impaired the recruitment of beta-arrestin to C
193 K6 reduced CXCL12-induced phosphorylation of Ser-346/7 with GRK3 knockdown having the strongest effec
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
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
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
211 in the receptor variants that lacked Lys or Ser/Thr residues, and the hD4R mutant that lacked 17 cyt
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
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
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
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
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
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
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
240 sphorylated SGT1 at four conserved residues (Ser-17, Ser-249, Ser-289, and Thr-233) and thereby preve
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
246 Together, these studies demonstrate the role Ser-346/7 plays in arrestin recruitment and initiation o
253 ts how phosphorylation of a regulatory site (Ser-500) integrates with Ca(2+) and CaM to influence eEF
256 CPKs are composed of a dual specificity (Ser/Thr and Tyr) kinase domain tethered to a calmodulin-
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
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
267 mpared with that of WT-YBX1, confirming that Ser-176 phosphorylation is critical for the activation o
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
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
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
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
295 Ser(261), Ser(264), and Thr(269)), of which Ser(256) is crucial and sufficient for AQP2 translocatio
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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