ライフサイエンスコーパス: protein kinase C-zeta

1 but not those of protein kinase C epsilon or protein kinase C zeta.

2 ), mammalian target of rapamycin (mTor), and protein kinase C-zeta.

3 PKCzeta (protein kinase C-zeta), a member of protein kinase C fam

4 neural progenitors was dependent on atypical protein kinase C zeta, a mediator of stem cell polarity,

5 termediate phosphatidylinositol 3 kinase and protein kinase C-zeta activation.

6 gands targeted to the atypical C1 domains of protein kinase C zeta and iota, we have prepared diacylg

7 es peroxynitrite production, which activates protein kinase C zeta and it's binding to the E3 SUMO (s

8 ng of F-actin polymerization also depends on protein kinase C zeta and protein kinase B (Akt/PKB).

9 e residue (Thr402) in the activation loop of protein kinase C-zeta and activated the enzyme in vitro

10 tidylinositol 3-kinase (PI3-K), Rho-GTPases, protein kinase C-zeta, and extracellular signal-regulate

11 lled CPC differentiation via integrin-beta1, protein kinase C-zeta, and v-akt murine thymoma viral on

12 ted, persistently active isoform of atypical protein kinase C-zeta (aPKCzeta), which lacks the N-term

13 The atypical protein kinase C isoform, protein kinase C-zeta, associates with and regulates the

14 The differential regulation of protein kinase C-zeta by enteropathogenic E. coli and en

15 specifically labeled, occludin itself, ZO-1, protein kinase C-zeta, c-Yes, the regulatory subunit of

16 induced HO-1 in endothelial cells through a protein kinase C zeta-dependent and vascular endothelial

17 st to enteropathogenic E. coli, the level of protein kinase C-zeta enzyme activity stimulated by ente

18 ), Rho-GTPases, Diaphanous-2 (Dia-2), Ezrin, protein kinase C-zeta, extracellular signal-regulated ki

19 e show a role for p38 MAPK and actin but not protein kinase C zeta in generating the respiratory burs

20 aim of this study was to compare the role of protein kinase C-zeta in the disruption of tight junctio

21 rrhagic E. coli was transient and minor, and protein kinase C-zeta inhibition had no effect on the de

22 62 is an interacting partner of the atypical protein kinase C zeta/iota and serves as a scaffold for

23 Furthermore, AKT, but not protein kinase C-zeta, is used by SCF/c-kit/PI3-K to act

24 the glutamate AMPA receptor and the atypical protein kinase C zeta isoform (PKMzeta).

25 s were unchanged, and the amount of atypical protein kinase C zeta/lambda (aPKC zeta/lambda), a prote

26 ociated kinase 1, Akt/PKB, ERK, and atypical protein kinase C zeta/lambda.

27 nt mice are at least in part due to impaired protein kinase C-zeta/lambda and AMP-kinase activities i

28 operates through the activation of atypical protein kinase C zeta, leading to GRK2-driven Galphas in

29 MGB1, whose release of HMGB1 induced a rapid protein kinase C zeta-mediated internalization of surfac

30 (TNF-alpha) or serum and stimulate atypical protein kinase C zeta (PKC zeta) activity, resulting in

31 BSEP promoter activity could be blocked with protein kinase C zeta (PKC zeta) inhibitors (pseudosubst

32 Protein kinase C zeta (PKC zeta) is a member of the PKC

33 e induction of apoptosis in mammalian cells, protein kinase C zeta (PKC zeta) is processed between th

34 y interacting directly and specifically with protein kinase C zeta (PKC zeta) isoform in renal cell c

35 ceramide selectively and directly activated protein kinase C zeta (PKC zeta) to suppress Akt-depende

36 Hypoxia promotes Na,K-ATPase endocytosis via protein kinase C zeta (PKC zeta)-mediated phosphorylatio

37 ositide-dependent kinase-1 (PDK-1), AKT, and protein kinase C zeta (PKC-zeta) in HepG2 and Huh7 cells

38 e Prkcz gene to generate mice that lack both protein kinase C-zeta (PKC-zeta) and PKM-zeta (Prkcz(-/-

39 -kinase, and another downstream kinase, e.g. protein kinase C-zeta (PKC-zeta) and/or protein kinase N

40 -linked phosphorylation of RelA at Ser311 by protein kinase C-zeta (PKC-zeta) blocked the binding of

41 Activation of protein kinase C-zeta (PKC-zeta) by insulin requires pho

42 ses in enzyme activity of immunoprecipitable protein kinase C-zeta (PKC-zeta) in rat adipocytes.

43 A protein kinase C-zeta (PKC-zeta) inhibitor (a pseudosubs

44 Protein kinase C-zeta (PKC-zeta) is a serine/threonine k

45 LDL treatment also elevated protein kinase C-zeta (PKC-zeta) phosphorylation and ind

46 Protein kinase C-zeta (PKC-zeta) plays a central role in

47 This effect was mediated by protein kinase C-zeta (PKC-zeta) since specific inhibiti

48 sphatidylinositol 3-kinase (PI 3-kinase) and protein kinase C-zeta (PKC-zeta) were recruited as upstr

49 A positive correlation between protein kinase C zeta (PKCzeta) activation and d-flow ha

50 We hypothesized that protein kinase C zeta (PKCzeta) activation by TNFalpha w

51 f the zeta isoform of PKC, and inhibition of protein kinase C zeta (PKCzeta) activity abrogated LPC-d

52 CaBP4 is phosphorylated by protein kinase C zeta (PKCzeta) at serine 37 both in vit

53 tudies have demonstrated that reduced T-cell protein kinase C zeta (PKCzeta) expression is associated

54 Atypical Protein Kinase C zeta (PKCzeta) forms Partitioning-defec

55 n and the role of NADPH oxidase 4 (Nox4) and protein kinase C zeta (PKCzeta) in mediating this respon

56 itro and insulin resistance in vivo activate protein kinase C zeta (PKCzeta) in pancreatic islets and

57 CaBP4 is phosphorylated by protein kinase C zeta (PKCzeta) in the retina at serine

58 Protein kinase C zeta (PKCzeta) inhibition before or 3 h

59 Atypical protein kinase C zeta (PKCzeta) is known to transduce si

60 We demonstrate that ceramide activation of protein kinase C zeta (PKCzeta) mediates SAPK signal com

61 tes a direct interaction between Galphaq and protein kinase C zeta (PKCzeta), leading to the stimulat

62 ck several protein kinase C isoforms but not protein kinase C-zeta, protected against the decrease in

63 coimmunoprecipitation of endogenous IRAK and protein kinase C-zeta protein.

64 e specific inhibitory peptide, myristoylated protein kinase C-zeta pseudosubstrate, also significantl

65 block novel and atypical isoforms, including protein kinase C-zeta, significantly attenuated the decr

66 rates the NADPH substrate, and by inhibiting protein kinase C zeta, which activates the NADPH oxidase

67 Likewise the inhibition of protein kinase C zeta, which is a known downstream effec