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1                                              p38beta is a 372-amino acid protein most closely related
2                                              p38beta MAPK down-regulated extracellular signal-regulat
3                                              p38beta-/- fibroblasts did not induce caveolin-1 in resp
4 zed a novel signaling pathway (MAPK kinase 6/p38beta MAPK/MAPKAP-K3) that defines a transcriptional m
5 ng mitogen-activated protein kinase kinase 6/p38beta mitogen-activated protein kinase/MAP kinase-acti
6 e show that estradiol (E2) rapidly activates p38beta mitogen-activated protein kinase in endothelial
7  Thus, we demonstrate that CO, by activating p38beta MAPK, up-regulates caveolin-1, which acts as a t
8                                       Again, p38beta was not detected in neutrophils, although low am
9 ate that SOCE activates CaMKKbeta-AMPKalpha1-p38beta MAPK signaling to phosphorylate STIM1, thereby s
10 the requirement of Rac1, MAPK kinase 3B, and p38beta for the full expression of NIS in MCF-7 cells.
11 induced AKT up-regulation in MCF-7 cells and p38beta MAP kinase activity in endothelial cells, blocke
12 ha MAPK, a regulator of DUX4 expression, and p38beta MAPK) for the treatment of facioscapulohumeral m
13 ed the reporter gene activation by IGF-I and p38beta MAPK significantly (p < 0.01).
14 onocytes; expression of p38delta was low and p38beta was undetected.
15  abolished, whereas the induction of p38 and p38beta was robust, but delayed.
16 d pathways are recruited to activate p38 and p38beta.
17 ock and sustained activation of p38alpha and p38beta accelerates osmostress-induced apoptosis.
18  addition, embryos lacking both p38alpha and p38beta also exhibit XY gonadal sex reversal.
19 BIRB796 than those that inhibit p38alpha and p38beta and at lower concentrations than those that inhi
20 2190 are specific inhibitors of p38alpha and p38beta and have been widely used in investigation of th
21 tress-activated protein kinases p38alpha and p38beta and is undergoing clinical trials for the treatm
22  PRAK activity was regulated by p38alpha and p38beta both in vitro and in vivo and Thr182 was shown t
23 T-cell receptor (TCR) activates p38alpha and p38beta by phosphorylation of p38 Tyr-323 (p38(Y323)).
24  the MAPK cascade and activates p38alpha and p38beta by phosphorylation of Tyr-323 and subsequent aut
25 mice to transient inhibition of p38alpha and p38beta in conjunction with culture on soft hydrogel sub
26              IL-1beta activated p38alpha and p38beta in endothelial cells.
27 KAPK5]) functions downstream of p38alpha and p38beta in mediating the signaling of the p38 pathway.
28                        Only the p38alpha and p38beta isoforms, but not the gamma or delta isoforms, c
29 on of SB202190, an inhibitor of p38alpha and p38beta MAPK activity, markedly increased the ability of
30 due to elevated activity of the p38alpha and p38beta mitogen-activated kinase pathway.
31 blast growth factor receptor-1, p38alpha and p38beta mitogen-activated protein kinase signaling in sa
32 ive small molecule inhibitor of p38alpha and p38beta mitogen-activated protein kinases (MAPKs) that i
33 ession of the dominant negative p38alpha and p38beta mutants.
34 nduces caspase-3 activation and p38alpha and p38beta phosphorylation suggesting that caspases and kin
35 ion and impaired the ability of p38alpha and p38beta to redistribute ectopically expressed PRAK, indi
36                            Only p38alpha and p38beta transcripts are ubiquitously expressed.
37           Using mice expressing p38alpha and p38beta with Y323F substitutions, we show that alternati
38 t contains a docking domain for p38alpha and p38beta, but it did not prevent the phosphorylation of A
39 03580, a compound that inhibits p38alpha and p38beta, but not the other p38 isoforms, can be used to
40 38 family members, specifically p38alpha and p38beta, in these processes has been difficult.
41 K3/p38gamma as well as those of p38alpha and p38beta.
42  or p38beta to the locations of p38alpha and p38beta.
43 by its docking interaction with p38alpha and p38beta.
44 negative forms of p38alpha (DN-p38alpha) and p38beta (DN-p38beta) MAPK were examined.
45 erfamily, in particular, JNKs, p38alpha, and p38beta MAPKs.
46 38 isoforms, p38alpha is proinflammatory and p38beta is cytoprotective.
47 otably, growth factor cytokine receptors and p38beta-mitogen-activated protein kinase (MAPK) were dif
48 nd that p38alpha accounts for two-thirds and p38beta the remainder of TCR-induced p38 activation.
49 Cre)-p38alpha(Delta/Delta) mice), as well as p38beta, gamma, and delta knockout.
50 d kinase inhibitor that preferentially binds p38beta MAPK, inhibited p300 activation 20-fold more pot
51 es, p38alpha and p38delta were abundant, but p38beta was undetected.
52 ances the promoter activity on activation by p38beta.
53 1 activation, which cannot be compensated by p38beta.
54 ncement of ATF2-dependent gene expression by p38beta was approximately20-fold greater than that of p3
55 ents showed a strong substrate preference by p38beta for activating transcription factor 2 (ATF2).
56 caveolin-1 expression, which was restored by p38beta gene transfer.
57  (also called RK/p38) or SAPK2b (also called p38beta) in activating MAPKAP kinase-2 and MAPKAP kinase
58 APK isoforms expressed in endothelial cells, p38beta knockdown prevented PAR-1-mediated STIM1 phospho
59                                 In contrast, p38beta was abundant in endothelial cells.
60             Compound transgenic DN-14-3-3/DN-p38beta mice, and to a lesser extent compound transgenic
61                           DN-p38alpha and DN-p38beta mice developed cardiac hypertrophy but were resi
62 N-p38alpha) or dominant-negative p38beta (DN-p38beta) MAPK expression was targeted to the heart.
63 ms of p38alpha (DN-p38alpha) and p38beta (DN-p38beta) MAPK were examined.
64 ctivated protein kinase (AMPK); its effector p38beta mitogen-activated protein kinase (p38beta MAPK)
65  as well as dominant negative constructs for p38beta or MKP-1.
66 a (STAT1alpha) and a 7.7-fold difference for p38beta phosphorylation of MK2.
67 hese findings reveal an in vivo function for p38beta and establish that MAPK signaling is essential f
68  against noninflammatory p38 isoforms (e.g., p38beta/MAPK11) and loss of all p38alpha-dependent respo
69                           On the other hand, p38beta is minimally expressed in early CD34(+) hematopo
70 itors in mice with a T106M point mutation in p38beta.
71 e phosphorylation of p38 isoforms, including p38beta.
72 hibitors, though the inhibitors also inhibit p38beta and perhaps some other enzymes.
73 kinase, the mitogen-activated protein kinase p38beta, mitogen- and stress-associated protein kinase-1
74 or p38beta mitogen-activated protein kinase (p38beta MAPK) phosphorylates STIM1, thus inhibiting SOCE
75       Here we characterize a new MAP kinase, p38beta.
76 catalyzed by MAPK kinases (MAPKKs), the MAPK p38beta is exceptional and is capable of self-activation
77 se (MAPK) family members, MAP3K1 and MAPK11 (p38beta), and the protein phosphatase 2 (PP2) subunit PP
78  of Toll-like receptor 4 in skeletal muscle, p38beta MAPK phosphorylates Ser-12 on p300 to stimulate
79                            Dominant negative p38beta protein expression decreased E2-mediated cardiom
80  p38alpha (DN-p38alpha) or dominant-negative p38beta (DN-p38beta) MAPK expression was targeted to the
81 ession vectors showed that p38alpha, but not p38beta, conferred 17,20 lyase activity on P450c17.
82 nstrated that p38alpha and p38gamma, but not p38beta, play an essential role in oncogenic ras-induced
83  design-targeted pockets in p38alpha but not p38beta.
84  of events associated with the activation of p38beta and p38 revealed differences, most notably in th
85 38alpha(-/-) cells, leading to activation of p38beta and p38gamma, which are not active in differenti
86  most notably in the preferred activation of p38beta by MAP kinase kinase 6 (MKK6), whereas p38 was a
87              IGF-I increased the activity of p38beta MAPK introduced into the cells by adenoviral inf
88  hypoxia had no effect on enzyme activity of p38beta, p38beta(2), p38delta, or on c-Jun N-terminal ki
89 he intrinsic autophosphorylation activity of p38beta.
90  and concomitantly augmented the activity of p38beta.
91              In contrast, HDX-MS analysis of p38beta did not detect significant temperature-dependent
92 ge, neutrophil, and T cell functions, and of p38beta to signaling in endothelial cells and T cells.
93 presses the intrinsic autophosphorylation of p38beta in mammalian cells.
94 the unique autophosphorylation capability of p38beta and the motif inhibiting this activity in living
95                                Expression of p38beta attenuated the apoptotic effect of SB202190 and
96                             The functions of p38beta and p38gamma in myoblast differentiation are not
97  cachexia due to its selective inhibition of p38beta MAPK.
98 se effects are reversed by the inhibition of p38beta, by the expression of a dominant-negative mitoge
99            Thus, p38alpha is an inhibitor of p38beta+p38gamma, which perhaps replace it in promoting
100  knockdown of p38alpha, but not knockdown of p38beta, inhibited 17,20 lyase activity in NCI-H295A cel
101                            Overexpression of p38beta or Rac1 significantly enhanced (1.9- and 3.9-fol
102 suppressed PAR-1-mediated phosphorylation of p38beta and hence STIM1.
103   In myogenic cell lines, phosphorylation of p38beta residue T241 is correlated with differentiation
104 hese findings demonstrate that prevention of p38beta MAPK-mediated activation of p300 by the FDA-appr
105 tent with the positive and negative roles of p38beta and p38delta in AP-1 regulation, MKK6 stimulates
106                                      T241 of p38beta is found phosphorylated in vivo in bone and musc
107 ugh a mechanism dependent on p38alpha and/or p38beta activation.
108 ng knock-in mice in which either p38alpha or p38beta kinase has been rendered resistant to the effect
109 nally, by selectively inhibiting p38alpha or p38beta MAPK isoforms, we demonstrate that p38alpha, rat
110 redistributed by coexpression of p38alpha or p38beta to the locations of p38alpha and p38beta.
111 A cells, suggesting an action on p38alpha or p38beta.
112                                    Like p38, p38beta is activated by proinflammatory cytokines and en
113 ion of JNK, followed by the induction of p38/p38beta at 3 days and ERK at 7 days.
114                                    p38alpha, p38beta, p38gamma, and p38delta are four isoforms of p38
115 There are four p38 family members (p38alpha, p38beta, p38gamma, and p38delta) that are activated by M
116  kinases (JNK1, JNK2, JNK3); p38s (p38alpha, p38beta, p38gamma, p38delta) and ERK5.
117                       We find that p38alpha, p38beta, and p38gamma are early activated by hyperosmoti
118                             Unlike p38alpha, p38beta was little affected by H/R.
119  Mutations in the docking groove on p38alpha/p38beta, or the p38-docking site in PRAK, disrupted the
120              Moreover, we show that p38alpha/p38beta and phosphoinositide 3-kinase are crucial to Tat
121 had no effect on enzyme activity of p38beta, p38beta(2), p38delta, or on c-Jun N-terminal kinase, ano
122 affect the activity of dually phosphorylated p38beta.
123  reduces the activity of T180-phosphorylated p38beta, and phosphorylation of T241 reduces its autopho
124 ted here suggest that while closely related, p38beta and p38 may be regulated by differing mechanisms
125     In addition, UBR2 up-regulation required p38beta-mediated phosphorylation of CCAAT/enhancer bindi
126    These results also suggest that selective p38beta agonists may represent attractive therapeutic ag
127                                   Similarly, p38beta knock-out mice respond normally to inflammatory
128 s, we demonstrate that p38alpha, rather than p38beta, MAPK activity is essential for uPA/uPAR express
129                             We conclude that p38beta is an unusual enzyme that automodulates its basa
130                          We demonstrate that p38beta mitogen-activated protein (MAP) kinase augments
131                           We discovered that p38beta also autophosphorylates in trans two previously
132 ther linked these signaling pathways in that p38beta was activated by E2 stimulation of PI3K.
133  antibody-induced arthritis, indicating that p38beta activity is not required for acute or chronic in
134                            Here we show that p38beta, a p38 isoform that is almost identical to p38al
135                                 We show that p38beta, but not AMPK, is likely to function upstream of
136                                          The p38beta does so by increasing the levels of phosphorylat
137                                          The p38beta isoform increases the activation of AP-1 transcr
138                                          The p38beta MAPK mediated the effects of CO on cytoprotectio
139 roliferation were similarly activated by the p38beta or inhibited by the p38gamma and/or -delta isofo
140 ation in cachectic muscle is mediated by the p38beta-C/EBPbeta signaling pathway responsible for the
141 ression of the p38alpha protein, but not the p38beta isoform, is suppressed in the brain.
142 dicated that tumor-induced activation of the p38beta isoform is sufficient and necessary for UBR2 up-
143                 Therefore, activation of the p38beta MAPK-C/EBPbeta signalling pathway appears a key
144                                        Thus, p38beta MAPK is a central mediator and therapeutic targe
145 e promoter activity is stimulated by LCM via p38beta-mediated activation of the C/EBPbeta-responsive
146 he effects of specific inhibitors along with p38beta knock-out mice to dissect the biological functio
147            Cotransfection of PC12 cells with p38beta and constitutively active MAPK kinase 6 resulted
148 ss only some of the p38 family members, with p38beta higher in 3T3 cells but p38delta only detected i

 
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