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1     This elevation depended on activation of p90 ribosomal S6 kinase.
2 ttenuated TPA-induced phosphorylation of ERK/p90 ribosomal S6 kinase.
3 so sufficient to activate both NF-kappaB and p90 ribosomal S6 kinase.
4 eviously we showed that the inactive form of p90 ribosomal S6 kinase 1 (RSK1) interacts with the regu
5                                              p90 ribosomal S6 kinase 1 (RSK1) is a serine/threonine k
6 ribosomal protein S6 kinase 1 (S6K1) but not p90 ribosomal S6 kinase 1 (RSK1) or Akt.
7  in cultured cells, interacts with mammalian p90 ribosomal S6 kinase 1 (RSK1), and causes a decrease
8 nt protein kinase (PKAc) binds to the active p90 ribosomal S6 kinase 1 (RSK1).
9 ERK1/2, and its dependent protein, p90RSK-1 (p90 ribosomal S6 kinase 1 or RSK-1), was abolished by me
10 iated activation of their direct target, the p90 ribosomal S6 kinase 1/2 (RSK1/2).
11                                              p90 ribosomal S6 kinase 2 (p90RSK2) is important in dive
12                  However, cells deficient in p90 ribosomal S6 kinase 2 (Rsk2(-/-)) totally block this
13 covered a novel regulatory mechanism whereby p90 ribosomal S6 kinase 2 (RSK2) interacts with 5-hydrox
14                                          The p90 ribosomal S6 kinase 2 (RSK2) is a serine/threonine k
15                        Here we show that the p90 ribosomal S6 kinase 2 (RSK2) phosphorylates actin-bi
16 ly, we discovered that the ERK/MAPK effector p90 ribosomal S6 kinase 2 (RSK2) phosphorylates the 5-HT
17      We report here that genetic deletion of p90 ribosomal S6 kinase 2 (RSK2) potentiates GPCR signal
18                         Here, we report that p90 ribosomal S6 kinase 2 (RSK2) promotes human HNSCC ce
19              We previously demonstrated that p90 ribosomal S6 kinase 2 (RSK2) promotes tumor metastas
20 nscriptional regulation, in which docking of p90 ribosomal S6 kinase 2 (Rsk2) to the hormone-binding
21 he activity of its downstream substrate, the p90 ribosomal S6 kinase 2 (RSK2), by 1.4-fold, but it ha
22                            We found that the p90 ribosomal S6 kinase 2 (RSK2)-cAMP response element-b
23  extracellular signal-regulated kinase 2 and p90 ribosomal S6 kinase 2 but not mitogen- and stress-ac
24  exercise protocol, MAPK phosphorylation and p90 ribosomal S6 kinase 2, MAP kinase kinase 1, and Raf-
25 he activity of its downstream substrate, the p90 ribosomal S6 kinase 2.
26                                          The p90 ribosomal S6 kinase-3 gene (p90 Rsk-3, RPS6KA2) maps
27                 The RPS6KA6 gene encodes the p90 ribosomal S6 kinase-4 (RSK4) that is still largely u
28 ctivated protein kinase phosphorylation, and p90 ribosomal S6 kinase activation, but did not affect t
29 nase C (PKC), but not by casein kinase II or p90 ribosomal S6 kinase, also activates PKA (7-fold).
30  mitogen-activated protein kinase (MAPK) and p90 ribosomal S6 kinase and consequent cell proliferatio
31 ing threonine 26 and serine 82, whereas PKC, p90 ribosomal S6 kinase, and casein kinase II, can phosp
32 ivo by isoforms of p70 S6 protein kinase and p90 ribosomal S6 kinase, and there is good evidence that
33 ts support the hypothesis that NF-kappaB and p90 ribosomal S6 kinase are involved in MEK5-ERK5-depend
34 induced phosphorylation of ERK1/2, CREB, and p90 ribosomal S6 kinase, as well as a decreased level of
35 not alter the TPA-induced phosphorylation of p90 ribosomal S6 kinase but caused a approximately 50% d
36  inhibition of the proteasome (by MG-132) or p90 ribosomal S6 kinases (by BI-D1870) is further increa
37 n in B cells was regulated by an ERK1/2- and p90 ribosomal S6 kinase-dependent mechanism, unlike in m
38                                          The p90 ribosomal S6 kinase family (RSK1-4) is a group of hi
39                                        RSKs (p90 ribosomal S6 kinases) have emerged as central regula
40 e p38 MAPK docking site of MAPKAPK2 converts p90 ribosomal S6 kinase into a stress-activated kinase i
41                                         RSK (p90 ribosomal S6 kinase) is a MAPK-activated protein kin
42 ble magnitude of phosphorylation of ERK-1/2, p90 ribosomal S6 kinase-l and Akt, although phosphorylat
43 rminal phosphorylation by p70 S6 kinases and p90 ribosomal S6 kinases on four conserved Ser residues
44      Protein kinase B (PKB), and the p70 and p90 ribosomal S6 kinases (p70 S6 kinase and p90 Rsk, res
45                    In addition, we show that p90 ribosomal S6 kinase (p90(RSK)) is a key NHE-1 kinase
46 ivate p70 ribosomal S6 kinase (p70(S6K)) and p90 ribosomal S6 kinase (p90(RSK)).
47 osomal S6 kinase 2 (RSK2) is a member of the p90 ribosomal S6 kinase (p90RSK) family of proteins and
48  serine/threonine kinase and a member of the p90 ribosomal S6 kinase (p90RSK) family of proteins.
49                                              p90 ribosomal S6 kinase (p90RSK) is activated in cardiom
50 ctor receptor (EGFR) that is coupled to MAPK/p90 ribosomal S6 kinase (p90RSK), but not phosphatidylin
51            MAPK and its downstream effector, p90 ribosomal S6 kinase (p90RSK), phosphorylate transcri
52 lly important downstream effector of PKCs is p90 ribosomal S6 kinase (p90RSK), which plays an importa
53 ant downstream effector of Src and ERK1/2 is p90 ribosomal S6 kinase (p90RSK), which plays an importa
54 hosphorylation of the known ERK1/2 substrate p90 ribosomal S6 kinase (p90RSK).
55     Here, we report the critical role of the p90 ribosomal S6 kinase (p90RSK)/ERK5 complex in EC dysf
56 PI3K/Akt or mitogen-activated protein kinase/p90 ribosomal S6 kinase pathways and subsequent tuberous
57 ated protein kinase (MAPK)-activated kinase, p90 ribosomal S6 kinase (RSK) 1, was found to interact w
58 iral proteins, ORF45, mediates sustained ERK-p90 ribosomal S6 kinase (RSK) activation during KSHV lyt
59 n CCT as a novel physiological substrate for p90 ribosomal S6 kinase (RSK) and p70 ribosomal S6 kinas
60         Here we report the identification of p90 ribosomal S6 kinase (RSK) as a target of salicylate.
61 ree enzymes that can phosphorylate GMF, only p90 ribosomal S6 kinase (RSK) enhances the inhibitory fu
62                                    While the p90 ribosomal S6 kinase (RSK) family has been implicated
63                                              p90 ribosomal S6 kinase (RSK) family members are effecto
64 pe I cAMP-dependent protein kinase (PKA) and p90 ribosomal S6 kinase (RSK) in cardiomyocyte apoptosis
65  The present study evaluated the function of p90 ribosomal S6 kinase (RSK) in the Drosophila circadia
66                                              p90 ribosomal S6 kinase (RSK) is an important downstream
67                          We demonstrate that p90 ribosomal S6 kinase (RSK) is recruited to the NFAT-D
68  involved in regulating transcription is the p90 ribosomal S6 kinase (RSK) isozyme, RSK2.
69 taining the carboxyl-terminal tails of three p90 ribosomal S6 kinase (RSK) isozymes (RSK1, RSK2, and
70 o regulate signaling through the Raf/MEK/ERK/p90 ribosomal S6 kinase (RSK) kinase cascade and show ho
71 af/MEK/extracellular signal-regulated kinase/p90 ribosomal S6 kinase (RSK) pathway.
72                                We found that p90 ribosomal S6 kinase (RSK) phosphorylated serine 703
73 ied extracellular regulated kinase (ERK) and p90 ribosomal S6 kinase (RSK) proteins, we found several
74                    In addition, depletion of p90 ribosomal S6 kinase (RSK) via siRSK1/2 completely ab
75                                          The p90 ribosomal S6 kinase (RSK), a cytosolic substrate for
76   tPA induced the phosphorylation of Erk1/2, p90 ribosomal S6 kinase (RSK), and p38 in a temporal ord
77 svirus (KSHV) causes sustained activation of p90 ribosomal S6 kinase (RSK), which is crucial for KSHV
78 te MAPK signaling by binding directly to the p90 ribosomal S6 kinase (RSK).
79 cribe a new negative regulator of IRS-1, the p90 ribosomal S6 kinase (RSK).
80 ent phosphorylation required the activity of p90 ribosomal S6 kinase (RSK).
81 osphorylation of serine 703 (Ser(P)(703)) by p90 ribosomal S6 kinase (RSK).
82 gated the role of the MEK kinase (MEKK)1/ERK/p90 ribosomal S6 kinase (RSK)1-dependent C/EBPbeta signa
83  kinase C (PKC), protein kinase B (PKB), p70/p90 ribosomal S6 kinases (RSK and S6K), and the catalyti
84 e demonstrate that DAPK is a novel target of p90 ribosomal S6 kinases (RSK) 1 and 2, downstream effec
85                                          The p90 ribosomal S6 kinases (RSK) are implicated in various
86 NTES induced phosphorylation of MEK, ERK1/2, p90 ribosomal S6 kinases (RSK), and cAMP-response elemen
87           ORF45 is a robust activator of the p90 ribosomal S6 kinases (RSK), and we found that this a
88  ERK leading to increased phosphorylation of p90-ribosomal S6 kinase (RSK) and a concomitant activati
89 lated by ERK via the "alternative" S6 kinase p90-ribosomal S6 kinase (RSK), as evidenced by the site
90                                              p90 ribosomal S6 kinase (RSK1) is an effector of both Ra
91 nd IL-15, but not IL-7, rapidly activate the p90 ribosomal S6 kinases, Rsk1 and Rsk2, in human T lymp
92 virus (KSHV), causes sustained activation of p90 ribosomal S6 kinases (RSKs) and extracellular regula
93 arcoma-associated herpesvirus interacts with p90 ribosomal S6 kinases (RSKs) and strongly stimulates
94                                          The p90 ribosomal S6 kinases (RSKs) are direct substrates of
95                                          The p90 ribosomal S6 kinases (RSKs) comprise a family of ser
96    The carboxyl-terminal domain (CTD) of the p90 ribosomal S6 kinases (RSKs) is an important regulato
97                                              p90 ribosomal S6 kinases (RSKs), containing two distinct
98 ed structure/function analysis of Drosophila p90 ribosomal S6 kinase (S6KII) or its mammalian homolog
99  extracellular signal-regulated kinase (ERK)/p90 ribosomal S6 kinase-signaling cassette.
100 s after phorbol ester stimulation in the ERK/p90 ribosomal S6 kinase-signaling targets, the tuberous
101 ate its substrates such as p70 S6-kinase and p90 ribosomal S6 kinase that do not interact with phosph
102 nt mechanism, unlike in macrophages in which p90 ribosomal S6 kinase was not required.
103     In addition, Raf-dependent activation of p90 ribosomal S6 kinase was only slightly impaired.
104 , extracellular signal-regulated kinase, and p90 ribosomal s6 kinase was suppressed by CPF or procyan
105 over, replacement of the ERK docking site of p90 ribosomal S6 kinase with the p38 MAPK docking site o
106 cardiac-specific overexpression of wild-type p90 ribosomal S6 kinase (WT-p90RSK-Tg) and a dominant-ne

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