ライフサイエンスコーパス: Raf-1 kinase

1 n from an active to an inactive state of the RAF-1 kinase.

2 e in R6 cells by enhancing activation of the Raf-1 kinase.

3 anine nucleotide exchange factor, Sos-1, and Raf-1 kinase.

4 14-3-3 proteins and 14-3-3 association with Raf-1 kinase.

5 nvolving inhibition of the Ras G-protein and Raf-1 kinase.

6 )-mediated phosphorylation and inhibition of Raf-1 kinase.

7 ation elicited by an oncogenically activated Raf-1 kinase.

8 s, i.e., Lyn and Jak2, and the activation of Raf-1 kinase.

9 ted in increased activity of ERK1, ERK2, and Raf-1 kinase.

10 disrupted the interaction of 14-3-3zeta with Raf-1 kinase.

11 e of the target genes activated by oncogenic Raf-1 kinase.

12 as found to interact with the protooncogenic Raf-1 kinase.

13 NaC) was identified as a target of activated Raf-1 kinases.

14 binding domain was found to be essential for Raf-1 kinase activation by each stimulus, including PMA.

15 -1 with the p50(cdc37)-Hsp90 heterodimer and Raf-1 kinase activation by serum.

16 tion, and insulin secretion, suggesting that Raf-1 kinase activation may be upstream to ERK1/2 and Ra

17 To determine whether Raf-1 kinase activation occurs at different concentratio

18 PKG activator, 8-pCPT-cGMPs, stimulated both Raf-1 kinase activity and endothelial proliferation in a

19 demonstrated that Raf-1 S471 is critical for Raf-1 kinase activity and for its interaction with mitog

20 we demonstrate a requirement for 14-3-3 for Raf-1 kinase activity and phosphorylation.

21 nent of the mechanism by which Ras activates Raf-1 kinase activity and that steady-state activated Ra

22 we demonstrate a novel single step assay for Raf-1 kinase activity based on phosphorylation of recomb

23 Reduced Raf-1 kinase activity in cells which expressed these NF1

24 induces increases in both proliferation and Raf-1 kinase activity in HUVECs and these activities are

25 assay, however, failed to detect LPS-induced Raf-1 kinase activity in RAW 264.7 cells, suggesting tha

26 ed, both tBHQ and SUL were able to stimulate Raf-1 kinase activity in vivo as well as in vitro.

27 These results establish that Raf-1 kinase activity is essential for cardiac hypertrop

28 oth C5b-9 and C5b-7, but not C5b6, increased Raf-1 kinase activity maximum 3.3-fold at 2 min and 2.8-

29 To examine the effects of Raf-1 kinase activity on the estrogen-dependent growth o

30 phorylation of Raf-1 on threonine, enhancing Raf-1 kinase activity toward MAP kinase kinase.

31 ate JAK2 kinase were also found to stimulate Raf-1 kinase activity toward MEK-1 in mammalian cells.

32 Moreover, Raf-1 kinase activity was greater in HIV-infected than u

33 VEGF-induced proliferation and Raf-1 kinase activity were also inhibited by Rp-8-pCPT-c

34 Some of these events modulate Raf-1 kinase activity while others determine interaction

35 However, gastrin stimulated Raf-1 kinase activity, and activation of the HDC promote

36 RANTES treatments activated Raf-1 kinase activity, and conversely a dominant negativ

37 t gastric ulceration significantly increases Raf-1 kinase activity, Grb2 and Ras protein, and Shc-Grb

38 Steel factor (SLF) synergistically stimulate Raf-1 kinase activity, protein synthesis, and proliferat

39 protein kinase C has been shown to activate Raf-1 kinase activity, the involvement of Raf-1 in pim-1

40 Raf-1 resulted in an overall decrease in the Raf-1 kinase activity.

41 growth factor (EGF)-induced sites, abolishes Raf-1 kinase activity.

42 ant, as we observe an NO-induced increase in Raf-1 kinase activity.

43 s that resulted in a significant decrease in Raf-1 kinase activity.

44 phorylation of Raf-1 at Ser-259 and impaired Raf-1 kinase activity.

45 Rheb interacts with and appears to regulate Raf-1 kinase, an essential component of the H-Ras signal

46 ed agents results in phosphorylation of both Raf-1 kinase and Bcl-2.

47 previously described PA binding segments of Raf-1 kinase and cyclic-AMP phosphodiesterase 4A1.

48 unctions in regulating interactions with the Raf-1 kinase and ERK activity.

49 shown that paclitaxel leads to activation of Raf-1 kinase and have suggested that this activation is

50 ng cells also exhibited a marked increase in Raf-1 kinase and MAP-kinase activity.

51 nd nucleus that was reduced by inhibitors of Raf-1 kinase and MEK-1/2.

52 A activity is required for activation of the Raf-1 kinase and that both Raf and KSR1 must be dephosph

53 ng dominant-negative constructs of p21(Ras), Raf-1 kinase, and mitogen-activated protein (MAP) kinase

54 ositive signaling induced activation of Ras, Raf-1 kinase, and mitogen-activated protein kinase; thes

55 pha substrates in MCF7-MDR cells: PKC-alpha, Raf-1 kinase, and P-glycoprotein.

56 ssion of constitutively active forms of Ras, Raf-1 kinase, and protein kinase C, all of which are act

57 An in vitro Raf-1 kinase assay, however, failed to detect LPS-induce

58 65 subunit of NF-kappaB or dominant negative Raf-1 kinase blocked insulin's induction of the mdr1b pr

59 Activation of Raf-1 kinase by paclitaxel is linked to tubulin polymeri

60 Furthermore, MAP kinase but not Raf-1 kinase catalytic activity is stimulated by FGFs.

61 cells expressing active mutants of H-Ras and Raf-1 kinase could also be reversed following Cdc2 inhib

62 (ii) Activation of an inducible Raf-1 kinase, DeltaRaf-1:estrogen receptor, resulted in

63 dy characterizes the interaction between the Raf-1 kinase domain and MEK1 and examines whether the ma

64 ase (PAK), and blocks phosphorylation of the Raf-1 kinase domain by PAK and Src family kinases.

65 Introduction of a mutationally activated Raf-1 kinase domain reversed tumor suppression by neurof

66 ody URP26K, which binds to an epitope in the Raf-1 kinase domain, inhibits intracellular signal trans

67 which, S471, is located in subdomain VIB of Raf-1 kinase domain.

68 ion site into the L12 activation loop of the Raf-1 kinase domain.

69 Bx caused the mitochondrial translocation of Raf-1 kinase either alone or in the context of whole-vir

70 ct (pRA-294-luc) and a constitutively active Raf-1 kinase expression vector (pRSV-Raf-BXB) resulted i

71 man C-raf-1 kinase to specifically inhibit C-raf-1 kinase gene expression and tumor progression in ce

72 on of TM is dependent on the activity of the Raf-1 kinase; however, the requirement for other downstr

73 with Raf-1 and results in the activation of Raf-1 kinase in a Ras-independent manner.

74 ovastatin blocked activation of p21(ras) and Raf-1 kinase in both 3T3-L1 fibroblasts and 3T3-L1 adipo

75 We have established a central role for Raf-1 kinase in regulating eosinophil survival, expressi

76 d the functional relevance of Lyn, Jak2, and Raf-1 kinases in eosinophil survival, upregulation of ad

77 ponents of the ERK pathway were inhibited by Raf-1 kinase inhibitor and the MEK inhibitor, PD98059.

78 Rituximab upregulates Raf-1 kinase inhibitor protein (RKIP) expression in non-

79 Raf-1 kinase inhibitor protein (RKIP) has been implicate

80 of the novel tumor and metastasis suppressor Raf-1 kinase inhibitor protein (RKIP) have been shown to

81 implicated a negative regulatory role of the Raf-1 kinase inhibitor protein (RKIP) on the ERK1/2 path

82 Rituximab significantly up-regulated Raf-1 kinase inhibitor protein expression, thus interrup

83 novel pathway mediated by rituximab through Raf-1 kinase inhibitor protein induction that negatively

84 essor/immunosurveillance cancer gene product Raf-1 kinase inhibitory protein (RKIP).

85 nstream targets of the metastasis suppressor Raf-1 kinase inhibitory protein (RKIP/PEBP1), we utilize

86 In this study we identify Raf-1 kinase inhibitory protein as an essential mediator

87 thermore, we show that either suppression of Raf-1 kinase inhibitory protein expression using short h

88 o ethanol induces protein kinase C-dependent Raf-1 kinase inhibitory protein phosphorylation, sensiti

89 ation of its novel interacting partner Rkip (Raf-1 kinase inhibitory protein).

90 t the cysteine-rich amino-terminal domain of Raf-1 kinase interacts selectively with phosphatidylseri

91 Raf-1 kinase is a key regulator of a number of cellular

92 The Raf-1 kinase is an important signaling molecule, functio

93 In contrast, Raf-1 kinase is critical for both these functions.

94 7 cells, suggesting that in RAW 264.7 cells, Raf-1 kinase is not an activating component of the LPS s

95 The Raf-1 kinase is regulated by phosphorylation, and Ser259

96 Downstream to Raf-1 kinase lie MAP kinases and their subsequent downst

97 that antisense inhibitors targeted against C-raf-1 kinase may be of considerable value as antineoplas

98 ytosolic serine/threonine kinases, including Raf-1 kinase, mitogen-activated protein kinase (MAPK), a

99 on of such important regulatory molecules as Raf-1 kinase, myristoylated alanine-rich C kinase substr

100 ebrafish embryos with RNA encoding wild-type Raf-1 kinase or a mutant version with triple alanine mut

101 ing either the p50/p65 NF-kappaB subunits or Raf-1 kinase or both resulted in increased expression of

102 Rho-GAP; expression of constitutively active Raf-1 kinase or MEK was sufficient to induce p190 Rho-GA

103 Both p21ras and its downstream Raf-1 kinase participate in the transduction of signals

104 d that mutual antagonism between the LPS and Raf-1 kinase pathways is not promoter specific, as the s

105 kinases phosphorylate and inactivate Rb, the Raf-1 kinase physically interacts with Rb and initiates

106 revious studies have shown that an inducible Raf-1 kinase protein, DeltaRaf-1:ER, activates the mitog

107 Specifically, a carboxyl-terminal domain of Raf-1 kinase (RafC; residues 295 648 of human Raf-1) int

108 not appear to be a significant mechanism of Raf-1 kinase regulation in COS-7 cells.

109 Activation of Raf-1 kinase resulted in a delayed and sustained increas

110 ed by transcription factor NF-kappaB via the Raf-1 kinase signaling pathway.

111 ntified a 35-amino acid segment within human Raf-1 kinase that preferentially binds phosphatidic acid

112 ansduction events, such as the activation of Raf-1 kinase, that may be essential for drug-induced apo

113 uiescent cells lead to the direct binding of Raf-1 kinase to Rb, leading to its inactivation.

114 igodeoxynucleotides targeted against human C-raf-1 kinase to specifically inhibit C-raf-1 kinase gene

115 Pharmacologic inhibition of Raf-1 kinase using GW-5074 markedly reduced the stimulat

116 l death, which could be delayed by activated Raf-1 kinase, was also seen in cells carrying the exogen

117 cted against the mitogenic signal transducer Raf-1 kinase, we investigated the elicited biological re

118 decreased the interaction of 14-3-3zeta with Raf-1 kinase, whereas R60E showed only subtle effects on