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1 PP1 activity is necessary for the induction of long-term
2 PP1 also associates with NCX1; however, the molecular ba
3 PP1 binds multiple motifs of DNA-PKcs, regulates DNA-PKc
4 PP1 did not change infarct size, electrocardiographic pa
5 PP1 first reactivates PP2A-B55; this enables PP2A-B55 in
6 PP1 has been found to be essential in Plasmodium falcipa
7 PP1 inhibition involves metal center oxidation rather th
8 PP1 interaction motifs within the Rif1 N-terminal domain
9 PP1 nuclear targeting subunit (PNUTS) is a PP1 targeting
10 PP1 pharmacological inhibitors would thus not be able to
11 PP1 plays critical roles in many essential physiological
12 PP1 raised Cx43 expression by 69% in the scar border (p
13 PP1 recruitment sets one or more critical thresholds for
14 PP1 recruitment to Cut12 sets a threshold for Polo's fee
15 PP1 recruitment to human, mitotic PP2A-B56 holoenzymes a
16 PP1 treatment restored active c-Src to sham levels at th
17 PP1-mediated dephosphorylation of Mps1 occurs at kinetoc
18 PP1-treated mice had restored conduction velocity at the
19 PP1/PP2A phosphatases counteracted this gradient and pro
20 regulators governing protein phosphatase 1 (PP1) activity have crucial functions because their delet
21 interactions between protein phosphatase 1 (PP1) and its regulator CPI-17, resulted in a reversible
22 sal in budding yeast, protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A) activities have e
24 o show that host cell protein phosphatase 1 (PP1) controls VP30 dephosphorylation because expression
25 The serine-threonine protein phosphatase 1 (PP1) deactivates this pathway whereas prolonging eIF2alp
26 The serine/threonine protein phosphatase 1 (PP1) dephosphorylates hundreds of key biological targets
28 proach, a recombinant protein phosphatase 1 (PP1) has been conjugated to MPs via coordination chemist
30 nd in Drosophila that Protein Phosphatase 1 (PP1) inactivates Mps1 by dephosphorylating its T-loop.
31 tment of GCs with the protein phosphatase 1 (PP1) inhibitor tautomycin increased phosphorylation of Y
32 (PPP1R1A) is a potent protein phosphatase 1 (PP1) inhibitor; however, its role in tumor development i
33 e protein phosphatase protein phosphatase 1 (PP1) is known to play an important role in learning and
35 genetic inhibition of protein phosphatase 1 (PP1) prevented HTTex1 aggregation in both human cells an
36 ly phosphorylates the protein phosphatase 1 (PP1) regulatory subunit myosin phosphatase targeting sub
37 omprising a catalytic protein phosphatase 1 (PP1) subunit in complex with a PPP1R15-type regulatory s
39 eriphery and recruits protein phosphatase 1 (PP1) to chromatin at anaphase onset, in a similar manner
41 domain (CTD) recruits protein phosphatase 1 (PP1) to kinetochores to promote timely anaphase onset [1
43 IGF-1R by activating protein phosphatase 1 (PP1) to promote dephosphorylation of inhibitory Ser/Thr
44 romote the binding of protein phosphatase 1 (PP1) to the p21(CIP1) promoter, leading to reduced H3S10
45 at functional CK2 and protein phosphatase 1 (PP1) were selectively tethered to the KCNQ2 subunit.
46 ed the interaction of protein phosphatase 1 (PP1) with the SR protein splicing factor (SRSF1) to unde
49 t Gwl associates with protein phosphatase 1 (PP1), particularly PP1gamma, which mediates the dephosph
50 d) and the associated protein phosphatase 1 (PP1), requiring NMDARcd movement, and persistently reduc
62 Serine/threonine protein phosphatase type-1 (PP1), a major phosphatase in the heart, consists of a ca
64 yl)-1H-pyrazolo[3,4-d]pyrimidin-4-amine (1NA-PP1) and 1-(tert-butyl)-3-(2-methylbenzyl)-1H-pyrazolo[3
67 ase 1/2), p38MAPK, protein phosphatase 1/2A (PP1/2A), and reactive oxygen species (ROS) were not invo
68 ld be blocked by a protein phosphatase 1/2A (PP1/PP2A) inhibitor and was partly blocked by a NMDA rec
69 yl)-1H-pyrazolo[3,4-d]pyrimidin-4-amine (2MB-PP1) but not by other 4-amino-5-(4-methylphenyl)-7-(t-bu
76 st that I-2, despite its assumed action as a PP1 inhibitor, is a positive regulator of PP1 function i
79 inal extension on yeast eIF2gamma contains a PP1-binding motif (KKVAF) that enables eIF2gamma to pull
80 ctivation of PP2A-B56 by dephosphorylating a PP1-docking site in PP2A-B56, thereby promoting the recr
82 PP1 nuclear targeting subunit (PNUTS) is a PP1 targeting protein that, with PP1, plays a central ro
83 30 dephosphorylation because expression of a PP1-binding peptide cdNIPP1 increased VP30 phosphorylati
85 he waning of stress responses and requires a PP1 catalytic subunit and a regulatory subunit, PPP1R15A
87 4) is induced downstream of ATF4, binds to a PP1-targeting subunit GADD34 at the endoplasmic reticulu
88 1alpha (PP1alpha) interacts with BRCA1 via a PP1-binding motif (898)KVTF(901), and can dephosphorylat
89 cal, yet novel mechanism, interacting with a PP1 pocket that is engaged only by these two PP1 regulat
92 we demonstrate that Rif1 is a high-affinity PP1 adaptor, able to out-compete the well-established PP
94 ed regulation between CaMKII (activator) and PP1 (inhibitor) and then the model performance was valid
95 ficance of the interaction between BRCA1 and PP1, and indicate that the K898E variant may render carr
102 ubR1-associated PP2A, unlike KNL1-associated PP1, plays a significant role in end-on conversion.
108 data also reveal that Ki-67 and RepoMan bind PP1 using an identical, yet novel mechanism, interacting
109 NA recognition motif 1 (RRM1) in SRSF1 binds PP1 and represses its catalytic function through an allo
111 ents by MPF and the NIMA kinase Fin1 blocked PP1(Dis2) recruitment, thereby promoting recruitment of
113 lation of eIF2alpha by interacting with both PP1 and eIF2alpha through independent binding motifs.
116 n of HTTex1 single phosphorylation events by PP1 could constitute an efficient and direct molecular t
117 ibutor to suppression of memory formation by PP1 may provide a novel therapeutic target for memory-re
119 measles V protein is mediated by a conserved PP1-binding motif in the C-terminal region of the V prot
120 enzymes and the sequences of these conserved PP1-docking motifs suggest that PP1 regulates PP2A-B55 a
126 g PP1, how they distinguish between distinct PP1 isoforms and how the assembly of these two holoenzym
127 hat, in contrast to the paradigm of distinct PP1-targeting or regulatory subunits, the unique N termi
128 P-32 to dampen Ca(2+) release by eliminating PP1 inhibition to enable it to dephosphorylate the InsP3
129 hat in anaphase, when the spindle elongates, PP1/Repo-Man promotes the accumulation of NuMA at the co
134 hrough a mechanism involving competition for PP1 molecules within the same macromolecular complex.
136 ntified a functional KVXF consensus site for PP1 binding in the N-terminal tail of KCNQ2 subunit: mut
138 n response to TNF, and this increased GADD34-PP1 phosphatase activity, dephosphorylating eukaryotic t
139 a adaptation pathway by inhibition of Gadd34-PP1 phosphatase with guanabenz protects oligodendrocytes
140 association of PP1 inhibitor I-1 with GADD34-PP1 holoenzymes, thereby inhibiting phosphatase activity
141 o signalling triggers assembly of the GADD34/PP1 complex in a negative feedback loop to inhibit Yap a
142 tion of the eIF2alpha holophosphatase GADD34:PP1, increases the phosphorylation of eIF2alpha in Schwa
143 tream aspects of synaptic signaling, but how PP1 activity is controlled in different forms of synapti
150 in PP1c-R-subunit interactions, which impair PP1 targeting to proteins involved in electrical and Ca(
151 s expressing a mutant V protein deficient in PP1 binding is unable to antagonize MDA5 and is growth i
153 ur work thus reveals a novel calcium-induced PP1 activation pathway critical for homeostatic synaptic
154 that the major effect of RSK-2 is to inhibit PP1 rather than to directly phosphorylate YB-1 on Ser(10
156 erived from the promiscuous kinase inhibitor PP1 to search for analogs that could potentially target
159 MI mice were treated with c-Src inhibitors (PP1 or AZD0530), PP3 (an inactive analogue of PP1), or s
161 4 at the endoplasmic reticulum, and inhibits PP1 activity to increase eIF2alpha phosphorylation and A
162 B kinase (Cdk1 also known as Cdc2) inhibits PP1 activity, but declining cyclin B levels later in mit
163 (low dose inhibits PP2A; high dose inhibits PP1) delayed AS160 Ser(588) (both doses) and Thr(642) (h
169 tivities of major protein phosphatases, like PP1 and PP2A, appear directly or indirectly repressed by
170 ortex at mid anaphase, kinetochore-localized PP1-Sds22 helps to break cortical symmetry by inducing t
175 ther show that platelets activate RhoA-MYPT1-PP1-mediated YAP1 dephosphorylation and promote its nucl
177 exclusively expressing the as-AurA with 1-Na-PP1, we discovered that Aurora A is required for central
179 pothesized that a direct and functional NCX1-PP1 interaction is a prerequisite for pSer-68-PLM dephos
180 ase (pat1-as2) by adding the ATP analog 1-NM-PP1 in G1-arrested cells allows the induction of synchro
181 87B or depletion of a conserved noncatalytic PP1 phosphatase subunit Sds22 leads to defects in p-moes
182 , okadaic acid (OA), and fostriecin, but not PP1 selective inhibitors, NIPP-1, and inhibitor 2, block
183 Furthermore, knockdown of PP1-alpha but not PP1-beta or PP1-gamma1 by small interfering RNA caused g
184 ur findings, we propose that Rif1 is a novel PP1 substrate targeting subunit that counteracts DDK-med
186 timulation in neurons leads to activation of PP1 through a mechanism involving inhibitory phosphoryla
188 nase Raf-1, which induces the association of PP1 inhibitor I-1 with GADD34-PP1 holoenzymes, thereby i
189 ermore, TNFalpha enhances the association of PP1 with GABA(A)R beta3 subunits and dephosphorylates a
190 calcineurin were involved in the control of PP1 activity in response to synaptic NMDA receptor stimu
193 g-term depression, whereas downregulation of PP1 activity is required for the normal induction of lon
194 e, p37 negatively regulates this function of PP1, resulting in lower cortical NuMA levels and correct
195 unclear how GLC7, the functional homolog of PP1 in yeast, is recruited to dephosphorylate eIF2alpha.
197 Furthermore, we found that inhibition of PP1/PP2A decreased HCN1 surface expression, whereas tyro
199 study, we aimed to analyze the mechanisms of PP1 targeting to the NCX1-pSer-68-PLM complex and hypoth
204 igned to impede MYPT1-mediated regulation of PP1, also decreased TEER in a reversible and non-toxic m
207 subunit (PNUTS), an inhibitory regulator of PP1, is also recruited to DNA damage sites to promote NH
209 a cytoplasm-shuttling regulatory subunit of PP1, and increased EBOV transcription, suggesting that c
214 ially Rb, by blocking their binding sites on PP1, insights that are providing strategies for selectiv
215 , knockdown of PP1-alpha but not PP1-beta or PP1-gamma1 by small interfering RNA caused greater AS160
220 isoforms of the ser/thr protein phosphatase PP1, is a mammalian-specific splice variant of the Ppp1c
221 ivities of SRPK1 and the protein phosphatase PP1, thereby regulating the phosphoryl content of the RS
223 ols cortical NuMA levels via the phosphatase PP1 and its regulatory subunit Repo-Man, but it acts ind
224 o-dependent expulsion of type-1-phosphatase (PP1) from the spindle pole by Fin1 (NIMA) kinase ensures
227 nal influence on type I protein phosphatase (PP1), likely resulting in negative regulation of cAMP/ca
228 eletal muscle serine/threonine phosphatases (PP1, PP2A, PP2B, and PP2C) on AS160 dephosphorylation.
234 eutic value of inhibition of the PKA/PPP1R1A/PP1 pathway in the treatment of primary and metastatic E
236 rus interact with PP1alpha/gamma, preventing PP1-mediated dephosphorylation of MDA5 and thereby its a
237 osome movement, may instead serve to promote PP1 recruitment to kinetochores fully attached to spindl
238 polymerization of the major Phloem Protein1 (PP1) and PP2, which correlated with a decline in carbony
239 henyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP1) analogs tested, whereas WT PKCdelta was insensitive
240 form mitotic exit phosphatases by recruiting PP1, how they distinguish between distinct PP1 isoforms
241 complex, specifically the Ska1 CTD, recruits PP1 to kinetochores to oppose spindle checkpoint signali
244 m different systems have suggested that Rif1-PP1 interaction is conserved and has important biologica
246 n velocity at the scar border (PP3: 32 cm/s, PP1: 41 cm/s, p < 0.05) and lower arrhythmic inducibilit
247 Recombinant inhibitor-2 protein (a selective PP1 inhibitor) delayed AS160 dephosphorylation on both p
250 PKA phosphorylation at Thr35, and subsequent PP1 binding and inhibition, was required for PPP1R1A-med
251 e regulatory subunits GADD34 and CReP target PP1 to dephosphorylate eIF2alpha; however, as there are
256 evealed that phosphatase activity other than PP1 continuously suppresses AurA(Thr-295) phosphorylatio
260 f this study was to test the hypothesis that PP1 is dysregulated in paroxysmal atrial fibrillation (P
261 tructure of the PP1:TTN complex reveals that PP1 selectivity is defined by a covalent bond between TT
262 ariety of molecular techniques, we show that PP1 catalytic subunit (PP1c) co-localized, co-fractionat
265 se conserved PP1-docking motifs suggest that PP1 regulates PP2A-B55 and PP2A-B56 activities in a vari
267 characterized AGC-family kinase Ypk3 and the PP1 phosphatase Glc7, whereas TORC2 regulates phosphoryl
269 A K898E germline missense variant in the PP1-binding motif of BRCA1 has been found in an Ashkenaz
270 ere we report that the lysine residue in the PP1-binding motif of BRCA1 is highly conserved across ma
271 , the structure shows how PNUTS inhibits the PP1-mediated dephosphorylation of critical substrates, e
274 and a targeted oxidative inactivation of the PP1 metal center, that sustains eIF2alpha phosphorylatio
276 in vitro affecting neither stability of the PP1-PPP1R15A complex nor substrate-specific dephosphoryl
280 ificity and the ability to predict how these PP1 interacting proteins bind PP1 from sequence alone is
283 o a PP1-binding peptide or fused directly to PP1 rescues mitotic defects caused by Ska1 depletion.
285 enhance gene expression in other cell types, PP1 activation to relieve IRS1 inhibition may be a more
286 e arginine site, allowed us to define unique PP1 binding motifs, which advances our ability to predic
290 Cdc42 signalling and suggest a way by which PP1/NIPP1 may contribute to the migratory properties of
291 escribe a mitotic phosphatase relay in which PP1 reactivation is required for the reactivation of bot
292 otic activation of Gwl, its association with PP1 is disrupted in mitotic cells and egg extracts.
300 PNUTS) is a PP1 targeting protein that, with PP1, plays a central role in the nucleus, where it regul
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