ライフサイエンスコーパス: p38beta

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 ed the reporter gene activation by IGF-I and p38beta MAPK significantly (p < 0.01).

13 onocytes; expression of p38delta was low and p38beta was undetected.

14 abolished, whereas the induction of p38 and p38beta was robust, but delayed.

15 d pathways are recruited to activate p38 and p38beta.

16 addition, embryos lacking both p38alpha and p38beta also exhibit XY gonadal sex reversal.

17 BIRB796 than those that inhibit p38alpha and p38beta and at lower concentrations than those that inhi

18 2190 are specific inhibitors of p38alpha and p38beta and have been widely used in investigation of th

19 tress-activated protein kinases p38alpha and p38beta and is undergoing clinical trials for the treatm

20 PRAK activity was regulated by p38alpha and p38beta both in vitro and in vivo and Thr182 was shown t

21 T-cell receptor (TCR) activates p38alpha and p38beta by phosphorylation of p38 Tyr-323 (p38(Y323)).

22 the MAPK cascade and activates p38alpha and p38beta by phosphorylation of Tyr-323 and subsequent aut

23 mice to transient inhibition of p38alpha and p38beta in conjunction with culture on soft hydrogel sub

24 IL-1beta activated p38alpha and p38beta in endothelial cells.

25 KAPK5]) functions downstream of p38alpha and p38beta in mediating the signaling of the p38 pathway.

26 Only the p38alpha and p38beta isoforms, but not the gamma or delta isoforms, c

27 on of SB202190, an inhibitor of p38alpha and p38beta MAPK activity, markedly increased the ability of

28 due to elevated activity of the p38alpha and p38beta mitogen-activated kinase pathway.

29 blast growth factor receptor-1, p38alpha and p38beta mitogen-activated protein kinase signaling in sa

30 ive small molecule inhibitor of p38alpha and p38beta mitogen-activated protein kinases (MAPKs) that i

31 ession of the dominant negative p38alpha and p38beta mutants.

32 ion and impaired the ability of p38alpha and p38beta to redistribute ectopically expressed PRAK, indi

33 Only p38alpha and p38beta transcripts are ubiquitously expressed.

34 Using mice expressing p38alpha and p38beta with Y323F substitutions, we show that alternati

35 t contains a docking domain for p38alpha and p38beta, but it did not prevent the phosphorylation of A

36 03580, a compound that inhibits p38alpha and p38beta, but not the other p38 isoforms, can be used to

37 38 family members, specifically p38alpha and p38beta, in these processes has been difficult.

38 K3/p38gamma as well as those of p38alpha and p38beta.

39 or p38beta to the locations of p38alpha and p38beta.

40 by its docking interaction with p38alpha and p38beta.

41 negative forms of p38alpha (DN-p38alpha) and p38beta (DN-p38beta) MAPK were examined.

42 erfamily, in particular, JNKs, p38alpha, and p38beta MAPKs.

43 otably, growth factor cytokine receptors and p38beta-mitogen-activated protein kinase (MAPK) were dif

44 nd that p38alpha accounts for two-thirds and p38beta the remainder of TCR-induced p38 activation.

45 Cre)-p38alpha(Delta/Delta) mice), as well as p38beta, gamma, and delta knockout.

46 es, p38alpha and p38delta were abundant, but p38beta was undetected.

47 ances the promoter activity on activation by p38beta.

48 1 activation, which cannot be compensated by p38beta.

49 ncement of ATF2-dependent gene expression by p38beta was approximately20-fold greater than that of p3

50 ents showed a strong substrate preference by p38beta for activating transcription factor 2 (ATF2).

51 caveolin-1 expression, which was restored by p38beta gene transfer.

52 (also called RK/p38) or SAPK2b (also called p38beta) in activating MAPKAP kinase-2 and MAPKAP kinase

53 APK isoforms expressed in endothelial cells, p38beta knockdown prevented PAR-1-mediated STIM1 phospho

54 In contrast, p38beta was abundant in endothelial cells.

55 Compound transgenic DN-14-3-3/DN-p38beta mice, and to a lesser extent compound transgenic

56 DN-p38alpha and DN-p38beta mice developed cardiac hypertrophy but were resi

57 N-p38alpha) or dominant-negative p38beta (DN-p38beta) MAPK expression was targeted to the heart.

58 ms of p38alpha (DN-p38alpha) and p38beta (DN-p38beta) MAPK were examined.

59 ctivated protein kinase (AMPK); its effector p38beta mitogen-activated protein kinase (p38beta MAPK)

60 as well as dominant negative constructs for p38beta or MKP-1.

61 hese findings reveal an in vivo function for p38beta and establish that MAPK signaling is essential f

62 against noninflammatory p38 isoforms (e.g., p38beta/MAPK11) and loss of all p38alpha-dependent respo

63 On the other hand, p38beta is minimally expressed in early CD34(+) hematopo

64 itors in mice with a T106M point mutation in p38beta.

65 e phosphorylation of p38 isoforms, including p38beta.

66 hibitors, though the inhibitors also inhibit p38beta and perhaps some other enzymes.

67 kinase, the mitogen-activated protein kinase p38beta, mitogen- and stress-associated protein kinase-1

68 or p38beta mitogen-activated protein kinase (p38beta MAPK) phosphorylates STIM1, thus inhibiting SOCE

69 Here we characterize a new MAP kinase, p38beta.

70 catalyzed by MAPK kinases (MAPKKs), the MAPK p38beta is exceptional and is capable of self-activation

71 Dominant negative p38beta protein expression decreased E2-mediated cardiom

72 p38alpha (DN-p38alpha) or dominant-negative p38beta (DN-p38beta) MAPK expression was targeted to the

73 ession vectors showed that p38alpha, but not p38beta, conferred 17,20 lyase activity on P450c17.

74 nstrated that p38alpha and p38gamma, but not p38beta, play an essential role in oncogenic ras-induced

75 design-targeted pockets in p38alpha but not p38beta.

76 of events associated with the activation of p38beta and p38 revealed differences, most notably in th

77 most notably in the preferred activation of p38beta by MAP kinase kinase 6 (MKK6), whereas p38 was a

78 IGF-I increased the activity of p38beta MAPK introduced into the cells by adenoviral inf

79 hypoxia had no effect on enzyme activity of p38beta, p38beta(2), p38delta, or on c-Jun N-terminal ki

80 he intrinsic autophosphorylation activity of p38beta.

81 and concomitantly augmented the activity of p38beta.

82 ge, neutrophil, and T cell functions, and of p38beta to signaling in endothelial cells and T cells.

83 presses the intrinsic autophosphorylation of p38beta in mammalian cells.

84 the unique autophosphorylation capability of p38beta and the motif inhibiting this activity in living

85 Expression of p38beta attenuated the apoptotic effect of SB202190 and

86 se effects are reversed by the inhibition of p38beta, by the expression of a dominant-negative mitoge

87 knockdown of p38alpha, but not knockdown of p38beta, inhibited 17,20 lyase activity in NCI-H295A cel

88 Overexpression of p38beta or Rac1 significantly enhanced (1.9- and 3.9-fol

89 suppressed PAR-1-mediated phosphorylation of p38beta and hence STIM1.

90 In myogenic cell lines, phosphorylation of p38beta residue T241 is correlated with differentiation

91 tent with the positive and negative roles of p38beta and p38delta in AP-1 regulation, MKK6 stimulates

92 T241 of p38beta is found phosphorylated in vivo in bone and musc

93 ugh a mechanism dependent on p38alpha and/or p38beta activation.

94 ng knock-in mice in which either p38alpha or p38beta kinase has been rendered resistant to the effect

95 nally, by selectively inhibiting p38alpha or p38beta MAPK isoforms, we demonstrate that p38alpha, rat

96 redistributed by coexpression of p38alpha or p38beta to the locations of p38alpha and p38beta.

97 A cells, suggesting an action on p38alpha or p38beta.

98 Like p38, p38beta is activated by proinflammatory cytokines and en

99 ion of JNK, followed by the induction of p38/p38beta at 3 days and ERK at 7 days.

100 p38alpha, p38beta, p38gamma, and p38delta are four isoforms of p38

101 kinases (JNK1, JNK2, JNK3); p38s (p38alpha, p38beta, p38gamma, p38delta) and ERK5.

102 Unlike p38alpha, p38beta was little affected by H/R.

103 Mutations in the docking groove on p38alpha/p38beta, or the p38-docking site in PRAK, disrupted the

104 Moreover, we show that p38alpha/p38beta and phosphoinositide 3-kinase are crucial to Tat

105 had no effect on enzyme activity of p38beta, p38beta(2), p38delta, or on c-Jun N-terminal kinase, ano

106 affect the activity of dually phosphorylated p38beta.

107 reduces the activity of T180-phosphorylated p38beta, and phosphorylation of T241 reduces its autopho

108 ted here suggest that while closely related, p38beta and p38 may be regulated by differing mechanisms

109 In addition, UBR2 up-regulation required p38beta-mediated phosphorylation of CCAAT/enhancer bindi

110 These results also suggest that selective p38beta agonists may represent attractive therapeutic ag

111 Similarly, p38beta knock-out mice respond normally to inflammatory

112 s, we demonstrate that p38alpha, rather than p38beta, MAPK activity is essential for uPA/uPAR express

113 We conclude that p38beta is an unusual enzyme that automodulates its basa

114 We demonstrate that p38beta mitogen-activated protein (MAP) kinase augments

115 We discovered that p38beta also autophosphorylates in trans two previously

116 ther linked these signaling pathways in that p38beta was activated by E2 stimulation of PI3K.

117 antibody-induced arthritis, indicating that p38beta activity is not required for acute or chronic in

118 Here we show that p38beta, a p38 isoform that is almost identical to p38al

119 We show that p38beta, but not AMPK, is likely to function upstream of

120 The p38beta does so by increasing the levels of phosphorylat

121 The p38beta isoform increases the activation of AP-1 transcr

122 The p38beta MAPK mediated the effects of CO on cytoprotectio

123 roliferation were similarly activated by the p38beta or inhibited by the p38gamma and/or -delta isofo

124 ation in cachectic muscle is mediated by the p38beta-C/EBPbeta signaling pathway responsible for the

125 ression of the p38alpha protein, but not the p38beta isoform, is suppressed in the brain.

126 dicated that tumor-induced activation of the p38beta isoform is sufficient and necessary for UBR2 up-

127 Therefore, activation of the p38beta MAPK-C/EBPbeta signalling pathway appears a key

128 e promoter activity is stimulated by LCM via p38beta-mediated activation of the C/EBPbeta-responsive

129 he effects of specific inhibitors along with p38beta knock-out mice to dissect the biological functio

130 Cotransfection of PC12 cells with p38beta and constitutively active MAPK kinase 6 resulted

131 ss only some of the p38 family members, with p38beta higher in 3T3 cells but p38delta only detected i