ライフサイエンスコーパス: MEK3

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1 3, but not Ser189, in the activation loop of MEK3.

2 cellular signal-regulated kinase kinase 3,6 (MEK3,6) activation and phosphorylation of p38.

3 This phenomenon was specific for MEK3,6, because these agents had no effect on the phosph

4 However, we found that a MEK3/6 --> p38 pathway contributes to SF-mediated activa

5 ugh inhibition of the Cys-containing targets MEK3/6 and TGF-beta-activated kinase 1 and of the JNK/SA

6 athways as examples, SMAD2/3, NOTCH1/2/3 and MEK3/6-p38 CPGs were found to regulate the signaling flo

7 s from either dysfunctional IKK/NF-kappaB or MEK3/6/p38/ATF-2 activation by IL-1.

8 -1 expression via both the IKK/NF-kappaB and MEK3/6/p38/ATF-2 pathways in astrocytes.

9 ts suggested that TAO2 selectively activates MEK3 and MEK6 but not MEKs 1, 4, or 7.

10 endogenous TAO2 specifically associates with MEK3 and MEK6 providing one mechanism for preferential r

11 ct interaction of p38delta with PKCdelta and MEK3 and show that exogenous agents that suppress kerati

12 novel protein kinase C isoforms, Ras, MEKK1, MEK3, and a p38delta-extracellular signal regulated kina

13 We demonstrate that LPS also activates MEK2, MEK3, and MEK6.

14 that the EGCG response requires Ras, MEKK1, MEK3, and p38 kinases.

15 ed by dominant-negative forms of Ras, MEKK1, MEK3, and p38.

16 that includes protein kinase C, Ras, MEKK1, MEK3, and p38/RK.

17 TAO1 activated MEK3 but not MEK4 or MEK6 in transfected cells.

18 (DND) (residues 220 to 340) associated with MEK3, but not PP2A, and its overexpression sensitized ce

19 The activation of and binding to MEK3 by TAO1 implicates TAO1 in the regulation of the p3

20 rotein kinase Cdelta (PKCdelta), Ras, MEKK1, MEK3 cascade that increases AP1 factor level and AP1 fac

21 MEK3 coimmunoprecipitated with TAO1 when they were expre

22 In addition, immunoreactive MEK3 endogenous to Sf9 cells copurified with TAO1 produc

23 kinase pathways in vitro and copurified with MEK3 endogenous to Sf9 cells.

24 ivity but not that of p38, ERK1 and ERK2, or MEK3, MEK4, or MEK6.

25 t negative forms of Ras, Raf-1, MEKK1, MEK1, MEK3, MEK7, ERK2, JNK1, and p38/RK inhibit the PMA-depen

26 nt negative forms of Ras, MEKK1, MEK1, MEK7, MEK3, p38/RK, and c-Jun inhibit the TPA-dependent increa

27 ited by dominant negative MEKK1, MEK1, MEK7, MEK3, p38/RK, and c-Jun.

28 marker, involucrin (hINV), via a Ras, MEKK1, MEK3, p38delta signaling cascade.

29 We propose that PKCdelta activates a MEKK1/MEK3/p38delta MAPK cascade to increase p53 levels and p5

30 que shift in MAPK activity via a Ras, MEKK1, MEK3 pathway, to increase p38 delta and inhibit ERK1/2 a

31 FLAG-alpha-4 coprecipitated hemagglutinin-MEK3 plus endogenous protein phosphatase 2A (PP2A) and s

32 A protein kinase C, Ras, MEKK1, MEK3 signaling cascade controls hINV expression by regul

33 s show that alpha-4 targets PP2A activity to MEK3 to suppress p38 MAPK activation by cytokines, there

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