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1 n oxidative stress independently of the Spc1 stress-activated protein kinase.
2 elta, or on c-Jun N-terminal kinase, another stress-activated protein kinase.
3 nt both on mitochondrial respiration and p38 stress-activated protein kinase.
4 PK), but not c-Jun N-terminal protein kinase/stress-activated protein kinase.
5 2alpha) on serine 51 is effected by specific stress-activated protein kinases.
6 gnaling was mediated by the p38 subfamily of stress-activated protein kinases.
7 feration and phosphorylation of mitogen- and stress-activated protein kinases.
8 8gamma in particular, and also p38alpha, two stress-activated protein kinases.
9 zipper transcription factor and a target for stress-activated protein kinases.
10 rtery cells is mediated by activation of the stress-activated protein kinases.
11 ly, protein kinase A (PKA), the mitogen- and stress-activated protein kinase 1 (MSK1) and the AMP-act
12 this study, we examined whether mitogen- and stress-activated protein kinase 1 (MSK1) is a downstream
13                                 Mitogen- and stress-activated protein kinase 1 (MSK1) is a growth-fac
14 ing an inactivating mutation of mitogen- and stress-activated protein kinase 1 (MSK1), a brain-derive
15 rminal "kinase-dead" mutants of mitogen- and stress-activated protein kinase 1 (MSK1), a downstream k
16 dy, we investigated the role of mitogen- and stress-activated protein kinase 1 (MSK1), a nuclear kina
17   ATF1 can be phosphorylated by mitogen- and stress-activated protein kinase 1 (MSK1), which is activ
18                           Here, mitogen- and stress-activated protein kinase 1 (MSK1), which itself i
19 in kinase (MAPK) activation and mitogen- and stress-activated protein kinase 1 (MSK1)-ranges of intra
20 els and also those of activated mitogen- and stress-activated protein kinase 1 (MSK1).
21  and activated by UVB-activated mitogen- and stress-activated protein kinase 1 (Msk1).
22 ence depend on an enzyme called mitogen- and stress-activated protein kinase 1 (MSK1).
23 osphorylates the nuclear kinase mitogen- and stress-activated protein kinase 1 (MSK1).
24 thways is the activation of the mitogen- and stress-activated protein kinase 1 (MSK1).
25 ells was not due to a defect in mitogen- and stress-activated protein kinase 1 or 90-kDa ribosomal S6
26         N- or C-terminal mutant mitogen- and stress-activated protein kinase 1 or its inhibitor H89 h
27 argets (ribosomal S6 kinase and mitogen- and stress-activated protein kinase 1) within the ventral te
28 0 ribosomal S6 kinase 2 but not mitogen- and stress-activated protein kinase 1.
29 ischemic phosphorylation of c-Jun N-terminal stress-activated protein kinase 1/2 (JNK1/2), p38, mitog
30  of the MAPK pathway results in mitogen- and stress-activated protein kinase 1/2 (MSK1/2)-catalyzed p
31 aB kinase-alpha (IKK-alpha) and Mitogen- and Stress-activated protein Kinases 1 and 2 (MSK1/2) have b
32 her, CREB1 was activated by the mitogen- and stress-activated protein kinases 1 and 2 (MSK1/2).
33 s shown to be mediated by RSK2, mitogen- and stress-activated protein kinase-1 (MSK1), and mitogen-ac
34 ibition of protein kinase A and mitogen- and stress-activated protein kinase-1 activity.
35  kinase, ribosomal S6 kinase-2, mitogen- and stress-activated protein kinase-1, p38 MAPK, phosphatidy
36 , alpha-PDGFR, but not beta-PDGFR, activates stress-activated protein kinase-1/c-Jun NH(2)-terminal k
37 ediated transformation through activation of stress-activated protein kinase-1/c-Jun NH2-terminal kin
38 ges triggered the activation of mitogen- and stress-activated protein kinases-1 and -2 (MSK1, MSK2) a
39  report that the MAPK family member known as stress-activated protein kinase-1c (SAPK1c, also known a
40 e (ERK) and the apoptotic/growth suppressive stress-activated protein kinase 2 (p38(MAPK)), and that
41 on formation and activation of FAK, Src, and stress-activated protein kinase 2, p38, were dysregulate
42 1/2 and p38 mitogen-activated protein kinase/stress-activated protein kinase 2.
43 d, tempo, but not tempol, potently activated stress-activated protein kinase (2 h, >3-fold).
44  protein kinases c-jun N-terminal kinase and stress-activated protein kinase-2.
45 y blocking the CA-4-P-mediated activation of stress-activated protein kinase-2/p38.
46  (71% over control) posttreatment, preceding stress-activated protein kinase activation and apoptosis
47 oxy-2-nonenal, have been reported to mediate stress-activated protein kinase activation and cell toxi
48 ne dithiocarbamate, markedly attenuated both stress-activated protein kinase activation and the induc
49  of the CD40ct is critical for NF-kappaB and stress-activated protein kinase activation, as well as t
50    Signals which upregulate Jun kinase (JNK)/stress-activated protein kinase activity also lead to as
51 oth LMPCD40 and LMP1 are now shown to induce stress-activated protein kinase activity in the absence
52 lysis of tobacco (Nicotiana tabacum) Osmotic Stress-Activated Protein Kinase activity in tobacco Brig
53             Rapid activation of p38, p44/42, stress-activated protein kinase and c-Jun N-terminal kin
54 associated verotoxins (VTs), VT1 and VT2, on stress-activated protein kinase and nuclear factor kappa
55 PK) superfamily, c-Jun amino-terminal kinase/stress-activated protein kinase and p38 MAPK.
56 nd activation of the c-Jun N-terminal kinase/stress-activated protein kinase and p38 pathways.
57 pha on the phosphorylation of JNK1/2 and p38 stress-activated protein kinase and their downstream tra
58 nd JNK/SAPK (c-Jun N-terminal protein kinase/stress-activated protein kinase)], and AKT.
59      CD40 ligation was known to activate the stress-activated protein kinase, and both LMPCD40 and LM
60 n of the protein kinases JNK1/2, ERK1/2, p38 stress-activated protein kinase, and mitogen-activated p
61 APKs: extracellular signal-regulated kinase, stress-activated protein kinase, and p38), protein phosp
62 on, or F-actin disruption, activated the JNK stress-activated protein kinase, and that interfering wi
63 -activated protein kinase 2 and mitogen- and stress-activated protein kinase are activated in psoriat
64  that Raf-1 interacts with the proapoptotic, stress-activated protein kinase ASK1 (apoptosis signal-r
65  role for Tpx1 in the activation of the Sty1 stress-activated protein kinase by peroxide, we find tha
66 ion of mitogen-activated protein kinases and stress-activated protein kinases by TNF and IL-1, sugges
67                                          The stress-activated protein kinase c-Jun N-terminal kinase
68 ligation, R-848 stimulated activation of the stress-activated protein kinases c-Jun kinase and p38 an
69 ts displayed higher levels of phosphorylated stress-activated protein kinase (c-jun N-terminal Kinase
70 used activation of c-Jun NH2-terminal kinase/stress-activated protein kinase, c-jun gene induction, a
71                                      Another stress-activated protein kinase, c-Jun N-terminal kinase
72                                          The stress-activated protein kinase, c-Jun N-terminal kinase
73 , was transiently phosphorylated and another stress-activated protein kinase, c-Jun NH(2)-terminal ki
74                In this study the role of the stress-activated protein kinases, c-Jun N-terminal kinas
75 ular signal-regulated kinases (ERK), and the stress-activated protein kinases, c-Jun NH2-terminal kin
76      Hypoxia (1% O2) stimulated strongly the stress-activated protein kinases, c-Jun NH2-terminal kin
77 associated with increased phosphorylation of stress activated protein kinase/c-Jun N-terminal kinase
78 xtracellular signal-regulated kinase 1/2 and stress activated protein kinase/c-jun N-terminal kinase,
79 he extracellular signal-regulated kinase and stress-activated protein kinase/c-Jun amino-terminal kin
80 r transcription factors NF-kappa B and AP-1, stress-activated protein kinase/c-Jun amino-terminal kin
81 tracellular signal-regulated kinase 1/2, and stress-activated protein kinase/c-Jun N-terminal kinase
82 llular signal-regulated kinase 1/2, p38, and stress-activated protein kinase/c-Jun N-terminal kinase
83 maging agents and regulates induction of the stress-activated protein kinase/c-Jun N-terminal kinase
84 otein kinase (MAPK), but not p44/42 (ERK) or stress-activated protein kinase/c-Jun N-terminal kinase
85 ich specifically associated with decrease in stress-activated protein kinase/c-Jun N-terminal kinase
86                               Phosphorylated stress-activated protein kinase/c-Jun N-terminal kinase
87 ase-1 (MEKK-1), an upstream activator of the stress-activated protein kinase/c-Jun N-terminal kinase
88 induced apoptosis was evaluated by measuring stress-activated protein kinase/c-jun N-terminal kinase
89 thout effect on the related kinase SAPK/JNK (stress-activated protein kinase/c-Jun N-terminal protein
90                                          The stress-activated protein kinase/c-Jun N-terminal protein
91 pable of activating c-jun expression include stress-activated protein kinase/c-Jun N-terminal protein
92  inhibition of PI3 kinase with wortmannin or stress-activated protein kinase/c-Jun NH(2)-terminal kin
93            However, TNF activation of p38 or stress-activated protein kinase/c-Jun NH(2)-terminal kin
94 nhibitors wortmannin and LY294002 stimulated stress-activated protein kinase/c-Jun NH(2)-terminal kin
95  and RANKL markedly potentiate NF-kappaB and stress-activated protein kinase/c-Jun NH(2)-terminal kin
96 and dominant negative mutants involving both stress-activated protein kinase/c-Jun NH(2)-terminal kin
97 ar regulated kinase 1 and 2 (ERK1/ERK2), and stress-activated protein kinase/c-Jun NH(2)-terminal kin
98  signal-regulated kinases 1/2, p38 MAPK, and stress-activated protein kinase/c-Jun NH(2)-terminal kin
99 gen-activated protein kinase, phosphorylated stress-activated protein kinase/c-Jun NH(2)-terminal kin
100 urative PDT increased phosphorylated p38 and stress-activated protein kinase/c-Jun NH(2)-terminal kin
101 ellular signal-regulated protein kinase 1/2, stress-activated protein kinase/c-JUN NH2-terminal kinas
102 llular signal-regulated kinase, p38 MAPK, or stress-activated protein kinase/c-Jun NH2-terminal kinas
103 kinase kinase kinases in pathways leading to stress-activated protein kinase/c-Jun NH2-terminal kinas
104 signal-regulated kinase (ERK), p38 MAPK, and stress-activated protein kinase/c-Jun-N terminal kinase)
105 lar signal-regulated kinase 1 and 2, p38 and stress-activated protein kinase/c-Jun-NH(2)-kinase were
106 ited the phosphorylation of Akt, Erk1/2, and stress-activated protein kinase/c-jun-NH(2)-kinase, with
107 EK) > SAPK/c-Jun NH(2)-terminal kinase (JNK) stress-activated protein kinase cascade and coordinately
108 ling via the JNK (c-Jun NH2-terminal kinase)/stress-activated protein kinase cascade to stimulate or
109 iated factor 2 (TRAF2) and activation of the stress-activated protein kinase cascade.
110 and of the JNK/SAPK (c-Jun N-terminal kinase/stress-activated protein kinase) cascade through inhibit
111 tor protein connection to IkappaB kinase and stress-activated protein kinases (CIKS)/Act1.
112 onse to HO-induced oxidative stress in a p38 stress-activated protein kinase-dependent manner.
113 previously reported substrate for DSP18, the stress-activated protein kinase, does not localize to mi
114 NO activated the extracellular-regulated and stress-activated protein kinases ERK, c-Jun NH(2)-termin
115 and Raf mutants but not by dominant-negative stress-activated protein kinase/ERK kinase and mitogen-a
116 ity and demonstrated an inhibitory effect on stress-activated protein kinase/ERK kinase-1 (SEK1); oth
117 nd -p90(RSK) and activation of p34(cdc2) and stress-activated protein kinase/ERK kinase/c-Jun N-termi
118  detected in the normal embryonic lens, this stress-activated protein kinase exhibited a robust activ
119                                         Both stress-activated protein kinase/extracellular signal-reg
120 tant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-reg
121           Concomitantly, Akt1 interacts with stress-activated protein kinase/extracellular signal-reg
122 vity; enhanced phosphorylation of SEK1/MKK4 (stress-activated protein kinase/extracellular signal-rel
123 e effects of CsA involve at least two of the stress-activated protein kinases (GCN2 and PERK) that ac
124 d protein kinase, NH(2)-terminal Jun kinases/stress-activated protein kinases, hexosamines, and other
125 nal osmolarity trigger the activation of the stress-activated protein kinase Hog1 (high-osmolarity gl
126     The yeast high-osmolarity glycerol (HOG) stress-activated protein kinase Hog1 is activated in res
127                                    The yeast stress-activated protein kinase Hog1 is best known for i
128               We conclude that inhibitors of stress-activated protein kinases improve the outcome of
129 .4 is the closest homolog of tobacco Osmotic Stress-Activated Protein Kinase in Arabidopsis (Arabidop
130 ation of hepatic c-Jun NH(2)-terminal kinase/stress-activated protein kinase in Cd39/Entpd1 mice afte
131 regulating the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase in cultured neurons.
132 ltistep phosphorelay system to the Spc1/Sty1 stress-activated protein kinase in the fission yeast Sch
133                       The function of PKN, a stress-activated protein kinase, in the heart is poorly
134                                Activation of stress-activated protein kinases, including the p38 and
135  increased the protein but not mRNA level of stress-activated-protein kinase interacting protein 1 (S
136                          p38 is an important stress activated protein kinase involved in gene regulat
137            The c-Jun N-terminal kinase (JNK)/stress activated protein kinase is preferentially activa
138                                          The stress-activated protein kinase JNK plays an important r
139                                Activation of stress-activated protein kinases JNK (and, to a lesser e
140                      C3 toxin stimulated the stress-activated protein kinases JNK and p38 and potenti
141 slation and the coordinate activation of the stress-activated protein kinases JNK and p38 MAPK.
142        Inhibition of c-Jun N-terminal kinase/stress-activated protein kinase (JNK) activity with the
143 in activation of the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and ERK1/2 MA
144 lated kinase Erk1/2, c-Jun-N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 MAPK,
145 ctivation of the c-Jun NH(2)-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38(MAPK)
146 monstrated to induce c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) cascade, whil
147 has been reported to activate the JUN kinase/stress-activated protein kinase (JNK/SAPK) pathway in mo
148                  The c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) pathway is ac
149 duction of the Jun N-terminal protein kinase/stress-activated protein kinase (JNK/SAPK) pathway was s
150 APK) and c-Jun NH(2)-terminal protein kinase-stress-activated protein kinase (JNK/SAPK) pathways upon
151 l also activates the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signal transd
152 ors, and activates the Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pat
153 chicine activate the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pat
154 hrough activation of c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), a signaling
155 nduced activation of c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and TRAF2 ca
156 s p38 MAP kinase and c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK).
157 ich binds to the c-Jun-NH(2)-terminal kinase/stress-activated protein kinases (JNK/SAPK).
158  genes c-jun and c-fos and activation of the stress-activated protein kinases, JNK/SAPK and p38, in t
159                       Chemical inhibition of stress-activated protein kinase/JNK showed that this MAP
160  in the pathway leading to c-Jun activation [stress-activated protein kinase/Jun N-terminal kinase (J
161 ated the phosphorylation of P38, P44/42, and stress-activated protein kinase/Jun N-terminal kinase (S
162                              Analysis of the stress-activated protein kinase/Jun N-terminal kinase (S
163                                              Stress-activated protein kinase kinase (SEK1), an upstre
164 n was blocked by transfections with either a stress-activated protein kinase kinase dominant-negative
165                                          JNK/stress-activated protein kinase kinase inhibition abroga
166 A for the dominant-negative mutant JNK-KR or stress-activated protein kinase kinase-1 Lys-->Arg mutan
167 (UV-B) triggers the activation of a group of stress-activated protein kinases known as c-Jun NH(2)-te
168 SK1 from 14-3-3zeta, and ASK1 then activates stress-activated protein kinases, leading to cell death.
169 o explants blocked activation of the p38 and stress-activated protein kinase MAPK and nuclear factor-
170  Hypoxia-reoxygenation activated the p38 and stress-activated protein kinase mitogen-activated protei
171 f c-Jun amino-terminal kinase (also known as stress-activated protein kinase), mitogen-activated prot
172                                 However, p38-stress-activated protein kinase-MK2 activation did not a
173 d human TTP function in both resting and p38-stress-activated protein kinase-MK2-activated cells.
174 netic approaches, we identified mitogen- and stress-activated protein kinases (MSKs) as primary media
175 s studies have established that mitogen- and stress-activated protein kinases (MSKs) regulate IL-10 p
176 tivation of c-Jun N-terminal kinase (JNK), a stress-activated protein kinase, on stress stimulation.
177 RGS7 by TNF-alpha requires activation of the stress-activated protein kinase p38 and the presence of
178 ygen species and mediates stimulation of the stress-activated protein kinase p38 MAPK downstream of t
179                                          The stress-activated protein kinase p38 plays a central role
180  activity by genotoxic stress is mediated by stress-activated protein kinase p38.
181 h increasing p62-dependent activation of the stress-activated protein kinase p38.
182        MKP5 dephosphorylates/inactivates the stress-activated protein kinase p38.
183                          Here we report that stress-activated protein kinases p38 and JNK trans-activ
184                  The inhibitor of the 38-kDa stress-activated protein kinase (p38(mapk)), SB 203580,
185 ulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase, p38, and Big MAP kinase
186 nner, but was sensitive to inhibition of the stress-activated protein kinase, p38.
187 sponse to insult occurs by signaling via the stress-activated protein kinases, p38, and c-Jun NH(2)-t
188 mitogen-activated protein kinase cascade and stress-activated protein kinase/p38, respectively, but i
189            The compound BIRB796 inhibits the stress-activated protein kinases p38alpha and p38beta an
190 e of immature MoDCs to LPS activates the p38 stress-activated protein kinase (p38SAPK), extracellular
191 2mapk/erk2, 2) p46 c-Jun NH2-terminal kinase/stress-activated protein kinase (p46 JNK/SAPK), and 3) p
192 ear Pmk1 by MAPK phosphatases induced by the stress activated protein kinase pathway is important for
193                             We show that the stress-activated protein kinase pathway (SAPK) and its e
194 lammation that include the activation of the stress-activated protein kinase pathway that, together w
195 by modulation of the c-Jun N-terminal kinase/stress-activated protein kinase pathway.
196 eceptors control the c-Jun N-terminal kinase/stress-activated protein kinase pathway.
197 ctivate the c-Jun N-terminal kinase (JNK, or stress-activated protein kinase) pathway.
198  GTPases, phosphatidylinositol 3-kinase, and stress-activated protein kinase pathways are not involve
199 tracellular K(+) and subsequent induction of stress-activated protein kinase pathways.
200 has been implicated in the activation of the stress-activated protein kinase pathways.
201 eIF2alpha) by the endoplasmic reticulum (ER) stress-activated protein kinase PERK modulates protein s
202 ibitors tested, only the inhibitor of JNK, a stress-activated protein kinase, potently blocked E. col
203 s 2/3, p38 mitogen-activated protein kinase, stress-activated protein kinase, protein kinase B, extra
204 d resulted in strong activation of eIF2alpha stress-activated protein kinase R-like endoplasmic retic
205 o study the mechanisms by which mitogen- and stress-activated protein kinases regulate cell cycle re-
206                                     The Hog1 stress-activated protein kinase regulates both stress re
207 ith Shiga toxin, synergistically upregulates stress-activated protein kinases, resulting in superindu
208 ukemia (CML), activates Ras and triggers the stress-activated protein kinase (SAPK or Jun NH2-termina
209 kinase kinases and an authentic substrate of stress-activated protein kinase (SAPK) 2a/p38.
210 hort-lived phosphorylation and activation of stress-activated protein kinase (SAPK) and cellular diff
211 Interestingly, DMS treatment induced the p38 stress-activated protein kinase (SAPK) and expression of
212 e show that ribosome collisions activate the stress-activated protein kinase (SAPK) and GCN2-mediated
213                                          The stress-activated protein kinase (SAPK) and mitogen-activ
214 n kinases, c-Jun amino-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and p38 mitogen-a
215 after treatment, and significantly activated stress-activated protein kinase (SAPK) and p38 mitogen-a
216 is accompanied by the activation of both the stress-activated protein kinase (SAPK) and p38 mitogen-a
217 ate DNA damage responses mediated by the p38/stress-activated protein kinase (SAPK) axis of signaling
218        We characterized participation of the stress-activated protein kinase (SAPK) cascade in the le
219 ytes by activating an upstream kinase in the stress-activated protein kinase (SAPK) cascade.
220                    We tested if mitogen- and stress-activated protein kinase (SAPK) cascades are invo
221 Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response t
222 se C (PKC) betaII-mediated activation of the stress-activated protein kinase (SAPK) pathway.
223                                              Stress-activated protein kinase (SAPK) pathways are evol
224 rs, the sphingomyelin and c-Jun Kinase (JNK)/Stress-activated Protein Kinase (SAPK) pathways have bee
225 minal kinase and p38 pathways, also known as stress-activated protein kinase (SAPK) pathways, are sig
226                  Therefore, not surprisingly stress-activated protein kinase (SAPK) pathways, pathway
227 In contrast, c-jun-NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) phosphorylation w
228         In eukaryotes, activation of JNK/p38 stress-activated protein kinase (SAPK) signaling pathway
229 restingly, SB203580, an inhibitor of the p38 stress-activated protein kinase (SAPK), and overexpressi
230  environmental stress stimuli is also called stress-activated protein kinase (SAPK), which has crucia
231  external hyperosmolarity activates the Hog1 stress-activated protein kinase (SAPK), which is a key p
232 alone had no effect on expression of phospho-stress-activated protein kinase (SAPK), wild-type p53, o
233 ignal-regulated kinase (ERK) kinase (MEKK) > stress-activated protein kinase (SAPK)-ERK kinase (SEK)
234 well as c-Jun amino-terminal kinase 1 (JNK1)/stress-activated protein kinase (SAPK).
235 of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).
236 or DLK activity and subsequent activation of stress-activated protein kinase (SAPK).
237 yeloma (MM) is associated with activation of stress-activated protein kinase (SAPK).
238 y a mechanism dependent on activation of the stress-activated protein kinase (SAPK).
239 knockdowns reduce TNF-mediated activation of stress-activated protein kinase (SAPK).
240 h RhoA-mediated actin remodeling and the p38 stress-activated protein kinase (SAPK).
241 sponse kinase (ERK), p-38 kinase (p-38), and stress-activated protein kinase (SAPK).
242  increased baseline levels of phosphorylated stress-activated protein kinase (SAPK)/c-jun NH(2)-termi
243 Here we describe the rapid activation of the stress-activated protein kinase (SAPK)/JNK pathway in BA
244 Chemotaxis toward ETs did not involve p38 or stress-activated protein kinase (SAPK)/Jun N-terminal ki
245 8 mitogen-activated protein (MAP) kinase and stress-activated protein kinase (SAPK)/Jun N-terminal ki
246 ceptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-termina
247 )1/2, p38, and c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK)] as well as serin
248 rotein kinase domain and that stimulates the stress-activated protein kinase (SAPK, also referred to
249                                          The stress-activated protein kinase (SAPK, alternatively JNK
250                            Activation of the stress-activated protein kinase (SAPK/JNK) by genotoxic
251 lta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells trea
252 C-terminus, has a specific activation of the stress-activated protein kinase (SAPK/JNK) pathway.
253 estly increased expression/activation of the stress-activated protein kinase (SAPK/JNK); moreover, SA
254 th the nuclear factor kappaB (NF-kappaB) and stress-activated protein kinase (SAPK; also known as c-J
255        In response to extracellular stimuli, stress-activated protein kinases (SAPK) modulate gene ex
256 es the N-terminal phosphorylation of ATF2 by stress-activated protein kinases (SAPK).
257  have identified a new Dictyostelium kinase (stress-activated protein kinase [SAPK]alpha), which is r
258  includes c-jun NH2-terminal kinase (JNK) or stress-activated protein kinase (SAPK1) and extracellula
259 ase cascades leading to enhanced activity of stress activated protein kinases (SAPKs), including JNK
260                    TNF-induced activation of stress activated protein kinases (SAPKs, Jun NH2-termina
261 ases (GCKs) and the subsequent activation of stress-activated protein kinases (SAPKs and c-Jun NH(2)-
262                                              Stress-activated protein kinases (SAPKs) are known to re
263                                              Stress-activated protein kinases (SAPKs) are stimulated
264             Regulation of gene expression by stress-activated protein kinases (SAPKs) is essential fo
265       The objective was to determine whether stress-activated protein kinases (SAPKs) mediated the tr
266 SR is known to involve the activation of the stress-activated protein kinases (SAPKs) p38 and JNK.
267 implex virus type 1 (HSV-1) can activate the stress-activated protein kinases (SAPKs) p38 and JNK.
268 t of the immediate upstream activator of the stress-activated protein kinases (SAPKs), abrogates the
269 c-Jun N-terminal kinases (JNKs), also called stress-activated protein kinases (SAPKs), belong to the
270 inase (JNK) activity, which involves JNKs or stress-activated protein kinases (SAPKs), is dependent o
271   In eukaryotic species from yeast to human, stress-activated protein kinases (SAPKs), members of a M
272                                              Stress-activated protein kinases (SAPKs), members of a m
273 fluorescence, resulting in the activation of stress-activated protein kinases (SAPKs), p38 MAPK, and
274         The relationship between PKR and the stress-activated protein kinases (SAPKs), such as p38 mi
275 nt on stress-induced nuclear accumulation of stress-activated protein kinases (SAPKs).
276            Induction of gene 33 requires the stress-activated protein kinases (SAPKs)/c-Jun NH(2)-ter
277                                          The stress-activated protein kinases (SAPKs, also called c-J
278  whereas that of AP-1/ATF can be mediated by stress-activated protein kinases (SAPKs; also named Jun
279 in kinase (MAPK) ERK-2, but did activate the stress-activated protein kinases (SAPKs; c-jun NH2-termi
280 r levels of hydroperoxide, and activates the stress-activated protein kinase (SEK) pathway.
281 tein kinase kinase 4 (MKK4), a member of the stress-activated protein kinase signaling cascade, has b
282 est that c-Jun and c-Jun NH2-terminal kinase/stress-activated protein kinase signaling may be involve
283 ively regulating the c-Jun N-terminal kinase/stress-activated protein kinase signaling pathway during
284       The effects of oxalate on mitogen- and stress-activated protein kinase signaling pathways were
285 t by the NF-kappaB and Jun N-terminal kinase/stress-activated protein kinase signaling pathways, two
286 attern of activation and deactivation of the stress-activated protein kinase signalling molecules c-J
287          Here we show that the fission yeast stress-activated protein kinase Sty1, a homolog of mamma
288 quired both Cdr1 autophosphorylation and the stress-activated protein kinase Sty1.
289                                        Other stress-activated protein kinases, such as ERK and p38, p
290             Jun N-terminal kinase (JNK) is a stress-activated protein kinase that can be induced by i
291 t PIKK family member, hSMG-1, as a genotoxic stress-activated protein kinase that displays some funct
292     AMP-activated protein kinase (AMPK) is a stress-activated protein kinase that is regulated by hyp
293                                     JNK is a stress-activated protein kinase that modulates pathways
294            Indeed, if JNK is considered as a stress-activated protein kinase, there appear to be mult
295 racellular-signal regulated kinases-1/-2 and stress-activated protein kinases, these enzymes did not
296 8 mitogen-activated protein (MAP) kinase nor stress-activated protein kinase was activated by [Ca(2+)
297                            Activation of p38 stress-activated protein kinase was required for LPS- or
298                       Phosphorylation of the stress-activated protein kinases was increased in both i
299 ctivity of the proapoptotic signal mediator, stress-activated protein kinase, was increased severalfo
300 DEP chemicals also induced the activation of stress-activated protein kinases, which play a role in c

 
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