ライフサイエンスコーパス: p38alpha

1 p38alpha bearing only a single phosphocysteine (pCys) as

2 p38alpha deficiency promoted monocyte proliferation but

3 p38alpha has a stronger effect, and it does so through h

4 p38alpha is a Ser/Thr protein kinase involved in a varie

5 p38alpha is a ubiquitous protein kinase strongly activat

6 p38alpha is activated by canonical upstream kinases that

7 p38alpha is essential for fibroblast activation and indu

8 p38alpha is phosphorylated first on Tyr-182 and then on

9 p38alpha knockout mice exhibited a 50% decrease in mean

10 p38alpha mitogen-activated protein (MAP) kinase is a mai

11 p38alpha mitogen-activated protein kinases (MAPK) may be

12 p38alpha phosphorylates P450c17 in a fashion that confer

13 p38alpha signaling in myeloid immune cells promoted IL-1

14 p38alpha through HuR stabilizes dnmt3a mRNA leading to a

15 p38alpha was activated and formed a disulfide-bound hete

16 p38alpha-deficient naive CD4(+) T cells preferentially d

17 p38alpha-knockout hepatocytes exhibited cytokinesis fail

18 ions in fibroblast growth factor receptor-1, p38alpha and p38beta mitogen-activated protein kinase si

19 ed TSH-stimulated phosphorylation of ERK1/2, p38alpha, and AKT1, whereas down-regulation of beta-arre

20 11(6H)-ones were synthesized and tested in a p38alpha enzyme assay for their inhibition of tumor necr

21 le transcription factor, was stabilized in a p38alpha- and NMD-dependent manner following persistent

22 nergic neuron somatic excitability through a p38alpha MAPK effect on GIRK deactivation kinetics rathe

23 Our studies have therefore uncovered a p38alpha-mediated pathway that alters HSPC metabolism to

24 lastogenesis and bone resorption by ablating p38alpha MAPK in LysM+monocytes.

25 on of substrate phosphorylation by activated p38alpha.

26 Biofilm PsaDM activated p38alpha MAPK in a Toll-like receptor-independent fashio

27 o injurious stimuli, biofilm PsaDM activated p38alpha MAPK strongly enough to recruit neutrophils, wh

28 Triptolide binds to and activates p38alpha and extracellular signal-regulated kinase 1/2 (

29 Upon satellite cell activation, p38alpha/beta MAPK phosphorylates MAPKAP2 and inactivate

30 orylation capability of intrinsically active p38alpha mutants, suggesting DEF-mediated trans-autophos

31 In addition, p38alpha activation helps tumor cells to survive chemoth

32 by TSH phosphorylates protein kinases AKT1, p38alpha, and ERK1/2 in some cells.

33 forms (e.g., p38beta/MAPK11) and loss of all p38alpha-dependent responses, including anti-inflammator

34 Although p38alpha in intestinal epithelial cells (IEC) plays an i

35 ignaling pathways centered on the ERK1/2 and p38alpha MAPK-interacting kinases MNK1/2 and their role

36 itors of c-Jun N-terminal kinase (JNK) 3 and p38alpha mitogen-activated protein (MAP) kinase.

37 ted between the expression of C/EBPalpha and p38alpha MAP kinase in tumor cells, suggesting that C/EB

38 response to RAF1 signaling and that ERK and p38alpha contribute to MSK1 activation in oncogene-induc

39 EF pocket), is formed subsequent to ERK2 and p38alpha activation.

40 nhibitors had high selectivity over JNK1 and p38alpha, minimal cytotoxicity, potent inhibition of 6-O

41 ir ability to inhibit both kinases, JNK3 and p38alpha MAP kinase.

42 ished in H9C2 cells expressing both MKK3 and p38alpha C119S/C162S and subjected to simulated ischemia

43 Thus, intermediates were MEK6/ST* and p38alpha/TY*.

44 nones, dibenzoxepines, and benzosuberones as p38alpha MAP kinase inhibitors.

45 ologically well interrogated kinases such as p38alpha (MAPK14) and ABL.

46 TGF-beta/p38alpha and NR4A1 also play essential roles in the indu

47 ample between p38alpha and HNF3, and between p38alpha and SOX9, and these are strongly supported by p

48 rmation of a protein:protein complex between p38alpha and mapkap kinases 2 and/or 3.

49 ntified by our analysis, for example between p38alpha and HNF3, and between p38alpha and SOX9, and th

50 he selective inhibition of the activation by p38alpha of the downstream kinase MK2 in preference to a

51 iometric phosphorylation events catalyzed by p38alpha and revealed that site 180 is a sufficient acti

52 control of signaling and gene expression by p38alpha.

53 inflammatory cytokines such as IFN-gamma by p38alpha-deficient T cells was reduced, which further re

54 xpressed human P450c17 was phosphorylated by p38alpha in vitro at a non-canonical site, conferring in

55 ll apoptosis is synergistically regulated by p38alpha isoform.

56 , CXCL2, CXCL10) are critically regulated by p38alpha signaling in astrocytes.

57 n, and tumorigenesis, as a gene regulated by p38alpha.

58 odulin-dependent protein kinase II (CaMKII), p38alpha mitogen-activated protein kinase (MAPK), and MA

59 n and nuclear translocation of the host cell p38alpha MAP kinase.

60 activation of the ROS-sensitive checkpoint, p38alpha.

61 9), a previously disclosed phase II clinical p38alpha MAP kinase inhibitor, a structurally novel clin

62 were negligible and limited by constitutive p38alpha MAPK activity, which was the main driver of pro

63 alpha MAPK inactivation blocked U50,488-CPA, p38alpha MAPK was not required for KOR inhibition of evo

64 ice where microglia were p38alpha-deficient (p38alpha KO) were protected against TBI-induced motor de

65 eptor activation required arrestin-dependent p38alpha MAPK activation in dopamine neurons but did not

66 specific deletion of GRK3/arrestin-dependent p38alpha MAPK from dopamine neurons blocked KOR-mediated

67 8alpha and serve as a platform for designing p38alpha-selective DEF site blockers, which partially in

68 own gene expression of mapk14, which encodes p38alpha MAPK, a kinase sensitive to inflammatory and ox

69 onal helix, alpha-helix 4, to further engage p38alpha.

70 from Lmna(H222P/H222P) mice showed enhanced p38alpha activation prior to and after the onset of hear

71 Mechanistically, loss of epithelial p38alpha signaling attenuates the expression of genes re

72 Although ERK1, p38alpha, p38beta2, and p38gamma were involved in induct

73 ese findings afford a new method to evaluate p38alpha and MK2/3 inhibitors within native biological s

74 Using mice expressing p38alpha and p38beta with Y323F substitutions, we show t

75 First, p38alpha is activated by TAB1 to phosphorylate p53 N-ter

76 nal genetic deletion of floxed KOR or floxed p38alpha MAPK by Cre recombinase expression in dopaminer

77 or little effect on pAKT1 (1.8+/-0.08-fold), p38alpha (1.2+/-0.09-fold), and pERK1/2 (1.6+/-0.19-fold

78 ls, TSH up-regulated pAKT1 (7.1+/-0.5-fold), p38alpha (2.9+/-0.4-fold), and pERK1/2 (3.1+/-0.2-fold),

79 lso illustrated protumorigenic functions for p38alpha.

80 Our findings demonstrate a key role for p38alpha in myeloid cells in CNS autoimmunity and uncove

81 We reveal a central role for p38alpha MAPK in establishing and maintaining such cross

82 inhibitors by a target hopping approach from p38alpha MAPK inhibitor templates.

83 insulate brain physiology and function from p38alpha-Mnk1-mediated signaling.

84 that in vivo responses to LPS after GFAPcre p38alpha deletion are complex and involve interactions b

85 tenuated astrogliosis in conditional GFAPcre p38alpha(-/-) mice.

86 However, GFAPcre p38alpha(-/-) mice showed marked upregulation of CCL2, C

87 roglia and neutrophil recruitment in GFAPcre p38alpha(-/-) mice compared to p38alphafl/fl controls.

88 Remarkably, the GRA24-p38alpha complex is defined by peculiar structural featu

89 and male-specific gene modules, with greater p38alpha dependence of proinflammatory gene expression i

90 specific transgenic mice to model heightened p38alpha disease signaling that occurs in dystrophic mus

91 Hence, p38alpha pro-migratory/invasive effect might be, at leas

92 However, the molecular mechanism how p38alpha controls immunomodulatory responses in myeloid

93 ation that lasted for at least 7 d; however, p38alpha KO mice failed to activate this response.

94 In clinical trials, however, p38alpha inhibitors produced adverse skin reactions and

95 cently reported 1a (skepinone-L) as a type I p38alpha MAP kinase inhibitor with high potency and exce

96 h was reduced and hepatomegaly was absent in p38alpha-deficient mice during chronic cholestasis throu

97 ng DEF-mediated trans-autophosphorylation in p38alpha.

98 otic index was very high upon cholestasis in p38alpha-deficient mice.

99 hese structural and energetic differences in p38alpha engagement highlight the fine-tuning necessary

100 ses of myeloid cells revealed differences in p38alpha-controlled transcripts comprising female- and m

101 ignificantly inhibits Th2 differentiation in p38alpha(-/-) T cells but not in p38alpha(+/-) T cells.

102 ildtype animals, whereas it remained high in p38alpha-deficient mice.

103 ained elevated in injured WT mice but not in p38alpha KO mice.

104 ntiation in p38alpha(-/-) T cells but not in p38alpha(+/-) T cells.

105 mputer-aided drug design-targeted pockets in p38alpha but not p38beta.

106 Cellular stress induced p38alpha-mediated mTOR activation that was independent o

107 In this study, we show that TGF-beta induces p38alpha (mitogen-activated protein kinase 14 [MAPK14]),

108 e DEF site blockers, which partially inhibit p38alpha binding DEF-dependent substrates, whereas maint

109 mutated form of KOR that could not initiate p38alpha MAPK activation did not.

110 nd chemokine levels was increased in injured p38alpha KO mice compared with injured WT mice.

111 When inserted into p38alpha, this fragment renders it spontaneously active

112 surprisingly found that CD8 T cell-intrinsic p38alpha activation was not responsible for increased su

113 and invasion in MEFs by mechanisms involving p38alpha/beta inhibition.

114 critical role for the p38MAPK family isoform p38alpha in initiating hematopoietic stem and progenitor

115 A or p50/NF-kappaB1) or the p38 MAPK isoform p38alpha prevented LPS-induced STIM1 expression and incr

116 outstanding biological activity on isolated p38alpha, with an IC50 value of 1.6 nM, extraordinary se

117 The best balanced dual JNK3/p38alpha MAP kinase inhibitors are 6m (IC50: JNK3, 18 nM

118 f the MAPK superfamily, in particular, JNKs, p38alpha, and p38beta MAPKs.

119 stimulation causes activation of NF-kappaB, p38alpha, and its downstream effector kinase MK2, thereb

120 The mitogen-activated protein kinase p38alpha (Mapk14 gene) is known to influence the cardiac

121 e show that activation of the protein kinase p38alpha is restricted to the epidermis in UVB-exposed s

122 ithelial-specific loss of the protein kinase p38alpha leads to aberrant activation of TAK1, JNK, EGF

123 The protein kinase p38alpha mediates cellular responses to environmental an

124 ylated the activation loop of protein kinase p38alpha.

125 The kinase p38alpha MAPK (p38alpha) plays a pivotal role in many bi

126 rosine kinase c-Src (Src) and Ser/Thr kinase p38alpha (p38), demonstrating broad applicability of the

127 3A, which is down-regulated in cells lacking p38alpha, but once re-introduced represses Fibulin 3 exp

128 showed that female but not male mice lacking p38alpha in myeloid cells exhibited reduced immune cell

129 Studies of mice lacking p38alpha in several different cell types have demonstrat

130 lated apoptosis-inducing ligand, Fas ligand, p38alpha mitogen-activated protein kinase, extracellular

131 Our data link p38alpha to mTOR signaling in myeloid immune cells that

132 In LSCs, p38alpha induces the expression of SDF-1, which activate

133 lective deletion of p38alpha in macrophages (p38alpha(DeltaLysM) ) were injected with K/BxN sera.

134 We found that in monocytes and macrophages, p38alpha activated the mechanistic target of rapamycin (

135 and deactivate the senescence-inducing MAPK p38alpha, belong to a group of redox-sensitive phosphata

136 The MAPK p38alpha senses environmental stressors and orchestrates

137 The kinase p38alpha MAPK (p38alpha) plays a pivotal role in many biological proces

138 ted and pharmacological silencing of Mapk14 (p38alpha) were found to sensitize mouse HCC to sorafenib

139 Deletion of Mapk14 (p38alpha-encoding gene) in the skeletal muscle of mdx- (

140 in part by directly regulating TEAD1, MAPK14/p38alpha and SERP1, factors involved in cell proliferati

141 reduces LPS-induced phosphorylation of MAPKs p38alpha and JNK1/2/3.

142 Mechanistically, p38alpha signaling increases expression of inosine-5'-mo

143 Moreover, p38alpha in CD103(+) DCs was required for optimal expres

144 omparing gene expression profiles of a mouse p38alpha (Mapk14) knock-out line to the original wild-ty

145 In the course of searching for new p38alpha MAP kinase inhibitors, we found that the regioi

146 kinase inhibitors are 6m (IC50: JNK3, 18 nM; p38alpha, 30 nM) and 14d (IC50: JNK3, 26 nM; p38alpha, 3

147 p38alpha, 30 nM) and 14d (IC50: JNK3, 26 nM; p38alpha, 34 nM) featuring both excellent solubility and

148 Our study illustrates a novel p38alpha-dependent mechanism preventing excessive genera

149 Our results reveal a novel p38alpha-dependent pathway that regulates NMD activity i

150 We predicted that Cys-119 or Cys-162 of p38alpha, close to the known MKK3 docking domain, were r

151 rk resulting from the presence or absence of p38alpha.

152 ition of Akt2 phosphorylation, activation of p38alpha and -gamma, and inhibition of proteasome activi

153 In this study, we show that activation of p38alpha in T cells is critical for the clearance of the

154 on factor 2-alpha) and ensuing activation of p38alpha kinase.

155 this study, we report that KOR activation of p38alpha MAPK in ventral tegmental (VTA) dopaminergic ne

156 metabolism gene expression and activation of p38alpha mitogen-activated protein kinase (p38).

157 DC subset contained constitutive activity of p38alpha and abundant expression of TGF-beta2 and retina

158 rotein 1 (TAB1), an activator of TAK1 and of p38alpha, associates with and inhibits the E3 ligase act

159 Deficiency of p38alpha in CD103(+) DCs inhibited the generation of ind

160 Mice deficient of p38alpha in T cells, but not in macrophages or dendritic

161 generated mice with conditional deletion of p38alpha (MAPK14) in GFAP+ astrocytes.

162 -molecule inhibition and genetic deletion of p38alpha and MK2 inhibit spontaneous but not induced sup

163 Deletion of p38alpha in DCs protected mice from T(H)17 cell-mediated

164 WT) mice and mice with selective deletion of p38alpha in macrophages (p38alpha(DeltaLysM) ) were inje

165 utoimmune neuroinflammation, but deletion of p38alpha in macrophages or T cells did not.

166 Conditional deletion of p38alpha led to defective recovery from hematological st

167 osure was blocked by conditional deletion of p38alpha MAPK, which also blocked KOR-induced tyrosine p

168 MAPKs, or by conditional genetic deletion of p38alpha MAPK.

169 inflammation, mice with induced deletion of p38alpha show elevated serum ovalbumin-specific IgE leve

170 ver, NO2-OA reduced the dephosphorylation of p38alpha by hematopoietic tyrosine phosphatase (HePTP).

171 These effects of p38alpha deficiency delineate a molecular network operat

172 Over-expression of p38alpha kinase down-regulated U6 promoter activity and

173 e lines genetically altered in expression of p38alpha, and mice in which p38alpha was deleted only in

174 as completely dependent on the expression of p38alpha.

175 D)] and dominant-negative [p38(DN)] forms of p38alpha.

176 dation of the context-dependent functions of p38alpha signaling in tumoral processes is of obvious im

177 liferation has been considered a hallmark of p38alpha-deficient cells.

178 Inhibition of p38alpha and ERK1/2 or p53 mutations could abolish the i

179 on from aged mice to transient inhibition of p38alpha and p38beta in conjunction with culture on soft

180 In all these cases, the inhibition of p38alpha has a potential therapeutic interest.

181 ased survival, but rather that inhibition of p38alpha in the Ag-presenting dendritic cells prevented

182 Inhibition of p38alpha MAPK also enhanced autophagy.

183 it was demonstrated that dual inhibition of p38alpha MAPK and PDE4 is able to synergistically attenu

184 ncidentally expanded to a dual inhibition of p38alpha MAPK and phosphodiesterase 4 (PDE4), and the po

185 highly selective small molecule inhibitor of p38alpha and p38beta mitogen-activated protein kinases (

186 Nevertheless, no inhibitor of p38alpha MAP kinase has been introduced to the market.

187 as blocked by a pharmacological inhibitor of p38alpha/beta mitogen-activated protein kinase (MAPK), S

188 This noncanonical kinetics of p38alpha activation correlates with the up-regulation of

189 and both p38 isoforms; however, knockdown of p38alpha, but not knockdown of p38beta, inhibited 17,20

190 e found to target and downregulate levels of p38alpha kinase, providing a specific survival signal fo

191 overed in our analysis as two novel links of p38alpha.

192 and cyclin B1 were up-regulated in liver of p38alpha-deficient mice upon chronic cholestasis, but un

193 phorylation was markedly reduced in liver of p38alpha-deficient mice upon chronic cholestasis.

194 Consequently, loss of p38alpha in DCs prevented induction of oral tolerance in

195 ol-5-amine led to an almost complete loss of p38alpha inhibition, but they showed activity against im

196 )) irradiation stimulates phosphorylation of p38alpha (MAPK14) by 5.78-fold, MSK2 (RPS6KA4) by 6.38-f

197 ASK1, and the subsequent phosphorylation of p38alpha by MEK6/S*T* (where S (Ser) and T (Thr) are the

198 The presence of p38alpha increases basal and H(2)O(2)-induced expression

199 mical methods, we observed that reduction of p38alpha MAPK expression facilitated the lysosomal degra

200 tumor cells is caused by down-regulation of p38alpha MAP kinase.

201 Our results highlight a key role of p38alpha in hepatocyte proliferation, in the development

202 Our aim was to assess the role of p38alpha in the progression of biliary cirrhosis induced

203 We studied the role of p38alpha signaling in astrocyte immune activation both i

204 important insights into the critical role of p38alpha signaling in astrocyte immune activation.

205 Consistent with a crucial role of p38alpha to program the tolerogenic activity of CD103(+)

206 te to understanding substrate selectivity of p38alpha and serve as a platform for designing p38alpha-

207 We also observed that silencing of p38alpha prevented c-Fos expression in response to LPS i

208 her CMGC protein kinases and a simulation of p38alpha.

209 ind competitively to the ATP binding site of p38alpha but unexpectedly with higher affinity in the p3

210 place preference behaviors by stimulation of p38alpha MAPK, which subsequently causes the translocati

211 Both crystal structures of p38alpha in its dually phosphorylated form and of intrin

212 Suppression of p38alpha protein was reversed by miR-124/-128 antisense

213 at in airway epithelial cells a threshold of p38alpha mitogen-activated protein kinase (MAPK) activat

214 d by evolution to allow for a fine tuning of p38alpha kinase activity.

215 and a new tool for improved understanding of p38alpha signaling pathways.

216 orylated in intrinsically active variants of p38alpha, but in this protein, they probably play a diff

217 The vulnerability of p38alpha-deficient epithelium predicts adverse effects o

218 cal HCI-H295A cells, suggesting an action on p38alpha or p38beta.

219 als from diverse modes of injury converge on p38alpha mitogen-activated protein kinase within the fib

220 nd invasion through a mechanism dependent on p38alpha and/or p38beta activation.

221 CT116 cells through a mechanism dependent on p38alpha, which surprisingly acts as a potent inducer of

222 plex results in a new probe labeling site on p38alpha that can be used to quantify the extent of inte

223 eads to an additional interaction surface on p38alpha.

224 Only p38alpha and p38beta transcripts are ubiquitously expres

225 We used a range of Asp-Phe-Gly (DFG)-in/out p38alpha mitogen-activated protein kinase inhibitors as

226 adverse effects of long term pharmacological p38alpha inhibition; yet such limitations could be overc

227 at Type II inhibitors inhibit phosphorylated p38alpha and allowed discovery of a predictive kinetic a

228 density dependent manner, with proliferating p38alpha(-/-) cultures showing increased differentiation

229 isoform-specific control of NOTCH2 promoter; p38alpha/beta2/delta, ERK1, and ERK2 contributed to cyto

230 component of the Mediterranean diet, reduced p38alpha activation and covalently modified Cys-119/Cys-

231 ced NF-kappaB activation, which may regulate p38alpha activation and IKKbeta-dependent IkappaBalpha d

232 Remarkably, p38alpha and PI3K concurrently modulated mTOR to balance

233 ch forms a negative feedback loop to repress p38alpha activation and promote cell survival upon UV ra

234 cytokines, including TGF-beta1, and requires p38alpha MAPK, but transcriptional mechanisms that under

235 s was induced in wildtype and liver-specific p38alpha knockout mice by bile duct ligation and animals

236 Moreover, monocyte-specific p38alpha ablation resulted in a decrease in bone formati

237 diffusible material (PsaDM) induced stronger p38alpha MAPK activation as compared to biofilm PsaDM.

238 mproved tolerability over previously studied p38alpha inhibitors.

239 region gave the opposite effect, suggesting p38alpha substrates can be classified into DEF-dependent

240 Targeted p38alpha depletion reduced Mnk1 activation, which cannot

241 the epidermis in UVB-exposed skin, and that p38alpha ablation targeted to the epithelial compartment

242 nditional deletion studies demonstrated that p38alpha signaling in macrophages/myeloid cells, but not

243 different cell types have demonstrated that p38alpha signaling is essential to maintaining the proli

244 Thus, our study demonstrates that p38alpha MAPK plays a critical role in the regulation of

245 In this study, we describe that p38alpha signaling in CD103(+) mesenteric lymph node DCs

246 deletion of the p38alpha gene, we find that p38alpha serves to limit NF-kappaB signaling and thereby

247 We also found that p38alpha orchestrated the expression of cytokines and co

248 here is good evidence in the literature that p38alpha plays an important tumor-suppressor role by int

249 ly demonstrated, using in vitro models, that p38alpha MAPK signaling in microglia is a key event in p

250 key glycosyltransferase genes revealed that p38alpha signaling was selectively required for inductio

251 Mechanistically, we show that p38alpha directly induces myofiber death through a mitoc

252 Here, we show that p38alpha kinase promotes EZH2 degradation in differentia

253 In this study, we show that p38alpha regulates gut-associated lymphoid tissue (GALT)

254 Here, we show that p38alpha, a kinase in the greater mitogen-activated prot

255 50c17 and p38 expression vectors showed that p38alpha, but not p38beta, conferred 17,20 lyase activit

256 Our research shows that p38alpha alone controls acute stress and cytokine signal

257 Together, these data suggest that p38alpha balances the inflammatory response by acutely a

258 n in response to LPS in ECs, suggesting that p38alpha signaling mediates the expression of c-Fos.

259 We describe here for the first time that p38alpha, p38gamma, and p38delta down-regulate fibulin 3

260 The p38alpha to p38delta mitogen-activated protein kinases (

261 itional Mapk14 allele was used to delete the p38alpha encoding gene specifically in cardiac fibroblas

262 s mainly of pharmacological experiments, the p38alpha MAP kinase isoform has been established as an i

263 However, the p38alpha C119S/C162S mutants did not exhibit appreciable

264 The increased cytokine levels in the p38alpha KO mice could not be accounted for by more infi

265 but unexpectedly with higher affinity in the p38alpha-MK2 complex compared with p38alpha alone.

266 target small molecules to a pocket near the p38alpha glutamate-aspartate (ED) substrate-docking site

267 rkers and is due to elevated activity of the p38alpha and p38beta mitogen-activated kinase pathway.

268 nal epithelial cell-specific deletion of the p38alpha gene, we find that p38alpha serves to limit NF-

269 egative ATG5 abolished the deficiency of the p38alpha MAPK-induced BACE1 protein reduction in culture

270 tent DNA damage required the activity of the p38alpha MAPK.

271 n be potently increased by inhibition of the p38alpha MAPK/MK2 signaling pathway.

272 This is mainly based on the ability of the p38alpha pathway to regulate tissue homeostasis by integ

273 We discovered that expression of the p38alpha protein, but not the p38beta isoform, is suppre

274 Similarly, the phosphorylation of the p38alpha transcription factor substrate ATF2 occurs in a

275 Manipulation of the p38alpha-TTP axis in macrophages has significant effects

276 rom these findings, we hypothesized that the p38alpha signaling pathway in microglia could be contrib

277 We also found that this p38alpha-dependent antioxidant response allows WT cells

278 ecreased the phosphorylation levels of three p38alpha substrates (ATFII, Elk-1, and MBP) with no appa

279 e extinguished C/EBPalpha expression through p38alpha inactivation leads tumor promotion and progress

280 Thus, p38alpha contributes to host defense against A/E pathoge

281 Thus, p38alpha MAPK is implicated in tumor angiogenesis throug

282 Thus, p38alpha signaling may facilitate the survival and proli

283 At the same time, p38alpha limits fibulin 3 expression, which might repres

284 This is due to p38alpha depletion by two neuron-selective microRNAs (mi

285 a, a p38 isoform that is almost identical to p38alpha, is exceptional and spontaneously autoactivates

286 Taken together, p38alpha regulates multiple T cell receptor-associated s

287 ) is involved in regulating EZH2 levels upon p38alpha activation.

288 dimesylate results were substantiated using p38alpha MAPK-specific shRNA and shRNA against the downs

289 ive signaling of both NF-kappaB and AP1 (via p38alpha) amplifies STIM1 expression in ECs and, thereby

290 Mice where microglia were p38alpha-deficient (p38alpha KO) were protected against

291 eterodimer-dependent probe labeling, whereas p38alpha inhibitors do not.

292 uncovered the molecular mechanisms by which p38alpha MAPK regulates osteoclastogenesis and coordinat

293 in expression of p38alpha, and mice in which p38alpha was deleted only in CD11c-expressing cells, we

294 family is composed of four kinases of which p38alpha/MAPK14 is the major proinflammatory member.

295 Surprisingly, while p38alpha MAPK inactivation blocked U50,488-CPA, p38alpha

296 ty in the p38alpha-MK2 complex compared with p38alpha alone.

297 on of the MAPK binding domain of DUSP16 with p38alpha and show that despite belonging to the same dua

298 uses a unique binding mode to interact with p38alpha.

299 may depend on redox-sensing cysteines within p38alpha.

300 ndings suggest that cysteine residues within p38alpha act as redox sensors that can dynamically regul