ライフサイエンスコーパス: G-kinase

1 nophosphate (cGMP)-dependent protein kinase (G-kinase).

2 arget gene vinculin was also blocked by cGMP/G-kinase.

3 pha(13)-induced Rho.GTP loading inhibited by G-kinase.

4 ntin filament organization via activation of G-kinase.

5 ls transfected with a catalytically inactive G-kinase.

6 c-Raf is the major target for regulation by G-kinase.

7 reover, the ability of insulin to inactivate GS kinase-3beta (GSK-3beta), the regulatory enzyme immed

8 cyclic GMP (cGMP)-dependent protein kinase (G-kinase) activates the human fos promoter in a strictly

9 G-kinase activation inhibited SRF-dependent transcriptio

10 nalogs is strictly dependent on G-kinase and G-kinase activation inhibits the Ras/MAP kinase pathway

11 was mediated by the CRE and proportional to G-kinase activity.

12 e cyclase and cGMP-dependent protein kinase (G-kinase) activity, and CS-54 arterial smooth muscle cel

13 e cyclase and cGMP-dependent protein kinase (G-kinase) activity.

14 cription by interfering with RhoA signaling; G-kinase acts both upstream of RhoA, inhibiting serum- o

15 G kinase also catalyzed the phosphorylation of peptides

16 t there were significant differences between G-kinase and A-kinase activation of single enhancer elem

17 wth by cGMP analogs is strictly dependent on G-kinase and G-kinase activation inhibits the Ras/MAP ki

18 functions in cancer-associated phenotypes (e.g., kinase and cell cycle).

19 43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected

20 The effect of G-kinase appeared to be mediated by several sequence ele

21 We identified a putative NLS in the G-kinase ATP binding domain which resembles the NLS of t

22 r elements requires nuclear translocation of G-kinase but not activation of mitogen-activated protein

23 xpression via cGMP-dependent protein kinase (G-kinase), but NO's precise mechanism of action is uncle

24 entration-dependent fashion, suggesting that G kinase catalyzes the phosphorylation of some proximal

25 ating our current findings with NOS, GC, and G kinase cycles is presented.

26 we report that transfection of G-kinase into G-kinase-deficient cells causes activation of the human

27 nase in G-kinase-expressing cells but not in G-kinase-deficient cells.

28 lular Ca(2+) waves, which were NO, cGMP, and G-kinase dependent, because incubating cells with nitric

29 al cells in a cGMP-dependent protein kinase (G-kinase)-dependent fashion.

30 esting regulation of C/EBP-beta functions by G-kinase-dependent dephosphorylation.

31 the fos promoter by a guanylate cyclase- and G-kinase-dependent mechanism.

32 G-kinase directly induced intermediate filament assembly

33 e and nuclear translocation of MAP kinase in G-kinase-expressing cells but not in G-kinase-deficient

34 Ras activation by EGF was not impaired in G-kinase-expressing cells treated with cGMP analogs.

35 ls co-transfected with guanylate cyclase and G-kinase expression vectors, CAT activity was increased

36 r analysis), or as functionally important (e.g., kinase fusions).

37 G-kinase had no effect on RhoA(63L)-induced morphologica

38 G-kinase had no effect on the high activation levels of

39 Soluble G-kinase I also regulates fos promoter activity, but mem

40 Our results suggest that G-kinase I and II control gene expression by different m

41 s mapped to the N-terminal 93 amino acids of G-kinase I beta and one of six 95-amino acid repeats fou

42 P analogs enhanced co-immunoprecipitation of G-kinase I beta and TFII-I by inducing co-localization o

43 we performed a yeast two-hybrid screen with G-kinase I beta as bait.

44 We found that G-kinase I beta interacted specifically with TFII-I, an

45 cally enhanced transcriptional activation by G-kinase I beta.

46 promoter activity, but membrane targeting of G-kinase I prevented the enzyme from translocating to th

47 location of cGMP-dependent protein kinase I (G-kinase I).

48 To identify nuclear targets of G-kinase I, we performed a yeast two-hybrid screen with

49 xtranuclear G-kinase II are not regulated by G-kinase I.

50 ll growth in cells stably transfected with a G-kinase Ibeta expression vector but not in untransfecte

51 empty vector or in cells transfected with a G-kinase Ibeta expression vector.

52 the transcriptional effects of extranuclear G-kinase II are not regulated by G-kinase I.

53 anslocate to the nucleus; however, a soluble G-kinase II mutant translocated to the nucleus and regul

54 The effect of G-kinase II on gene expression did not require calcium u

55 O effects on neuronal plasticity may involve G-kinase II regulation of gene expression.

56 G-kinase II was membrane associated and did not transloc

57 ave no effect; (3) CREB is phosphorylated by G-kinase in vitro and its phosphorylation increases in v

58 phorylation of the hepatic InsP3 receptor by G-kinase increases the sensitivity to InsP3 for [Ca2+]i

59 Activation of G-kinase induced MAP kinase phosphatase 1 expression, bu

60 We show that activation of G-kinase inhibited c-Raf kinase activation and that G-ki

61 c fashion with ROK being the most efficient; G-kinase inhibited transcription induced by all three ef

62 eficient VASP mutant can partly prevent cGMP/G-kinase inhibition of serum- and RhoA-induced SRE-depen

63 We now show that the G-kinase inhibition that occurs downstream of RhoA can b

64 nses to cGMP analogues were inhibited by the G-kinase inhibitor 8-bromoguanosine-3',5'-cyclic monopho

65 itric oxide synthase, guanylate cyclase, and G-kinase inhibitors, or NO scavengers, reduced Delta[Ca(

66 f cell function by NO in which activation of G kinase inhibits signaling by G protein-coupled recepto

67 We conclude that G-kinase inhibits SRF-dependent transcription by interfe

68 Cyclic GMP-dependent protein kinase (G-kinase) inhibits RhoA activation of SRE-dependent tran

69 Here we report that transfection of G-kinase into G-kinase-deficient cells causes activation

70 d its phosphorylation increases in vivo when G-kinase is activated either directly by cGMP or indirec

71 esults indicate that nuclear localization of G-kinase is required for transcriptional activation of t

72 gle amino acid residue (K407-->E) within the G-kinase NLS produced an enzyme with normal cGMP-depende

73 Fusion of the G-kinase NLS to the N terminus of beta-galactosidase pro

74 e inhibited c-Raf kinase activation and that G-kinase phosphorylated c-Raf kinase on Ser43, both in v

75 G-kinase phosphorylated TFII-I in vitro and in vivo on S

76 patic type-1 InsP3 receptor, indicating that G-kinase phosphorylates the InsP3 receptor at sites targ

77 RhoA can be explained, at least in part, by G-kinase phosphorylation of VASP on Ser(239) at the carb

78 (ii) did not require cytosolic components, e.g., kinases, proteases, phosphatases, etc., because it o

79 lating SRE-dependent transcription, and that G-kinase regulates VASP activity.

80 for the cGMP/cGMP-dependent protein kinase (G-kinase) signal transduction pathway.

81 Results from this study suggest that NO-G-kinase signaling is coupled to Ca(2+) mobilization and

82 e (100-200 microM) and antagonists of the NO-G-kinase signaling pathway essentially abrogated the NO-

83 ryanodine receptor-linked store, via the NO-G-kinase signaling pathway.

84 tric oxide-cGMP-dependent protein kinase (NO-G-kinase) signaling pathway in glial intercellular Ca(2+

85 G-kinase strongly enhanced TFII-I transactivation of a s

86 EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major ta

87 cell types containing cytoplasmic TFII-I the G-kinase-TFII-I interaction was largely cGMP-independent

88 press type II cGMP-dependent protein kinase (G-kinase); the effect on the fos promoter was mediated b

89 Similarly, B-Raf kinase was not inhibited by G-kinase; the Ser43 phosphorylation site of c-Raf is not

90 Binding of G-kinase to TFII-I may position the kinase to phosphoryl

91 The magnitude of G-kinase transactivation of the fos promoter was similar

92 Our results indicate that G-kinase transduces signals to the nucleus independently

93 Here, we demonstrate that G-kinase translocates to the nucleus by an active transp

94 Immunofluorescent staining of G-kinase was predominantly cytoplasmic in untreated cell

95 deficient in cGMP-dependent protein kinase (G-kinase), we show that 8-(4-chlorophenylthio)guanosine-

96 Nanomolar concentrations of G kinase were found to catalyze the phosphorylation of p

97 and activates cGMP-dependent protein kinase (G kinase), which by an unknown mechanism leads to inhibi

98 that type II cGMP-dependent protein kinase (G-kinase), which is widely expressed in the brain, media

99 contrast, N-terminally truncated versions of G-kinase with constitutive, cGMP-independent activity in