ライフサイエンスコーパス: G-alpha-q

1 G alpha q mRNA levels were down-regulated by 30% after 4

2 activate platelets deficient in PLC gamma 2, G alpha q, or TxA2 receptors, as well as platelets treat

3 [35S]G alpha i and [35S]G alpha q were immunoprecipitated from PF membranes incu

4 NTS1 monomers activate G alpha q beta(1)gamma(2), whereas receptor dimers catal

5 Activated G alpha q, as well as G alpha 12 and G alpha 13, coopera

6 larly, expression of a constitutively active G alpha q mutant, but not the wild-type G alpha q, led t

7 hypertrophy, whereas a constitutively active G alpha q subunit (GqQ209L) induces apoptosis.

8 Specific antisera directed against G alpha q and G alpha o but not G alpha s and G alpha i

9 Basal activity and G alpha q-dependent activation of the enzyme were unaffe

10 depression (depressed +dl/dt and -dl/dt) and G alpha q-25 hearts showed a pattern of fetal gene expre

11 We show that G alpha s, G alpha i3 and G alpha q/11 are present in Golgi fractions which are >

12 ns by immunoblotting, whereas G alpha i3 and G alpha q/11 were broadly distributed across Golgi fract

13 through a mechanism involving G alpha o and G alpha q.

14 insulin receptor substrates IRS-1, SHC, and G alpha q/11.

15 l-evoked membrane recruitment of tubulin and G alpha q transactivation by tubulin.

16 id not significantly change in aortic-banded G alpha q-25 mice.

17 Three weeks after transverse aortic banding, G alpha q-25 left ventricles hypertrophied to a similar

18 d the stimulation of PLC-beta(1) activity by G alpha q but had little effect on the stimulation by be

19 In transgenic mice with cardiac G alpha q overexpression, heart failure and increased ca

20 also induced a significant loss in cellular G alpha q/G alpha 11 levels.

21 o Ang II induces down-regulation of cellular G alpha q/G alpha 11 levels in intact VSMC.

22 , which concurrently down-regulated cellular G alpha q/G alpha 11 levels.

23 y dependent upon co-expression of a chimeric G alpha q/alpha i subunit, which confers Gq-effector cou

24 In contrast, G alpha q expression levels were significantly lower in

25 ed protein kinase family by GTPase-deficient G alpha q and G alpha 16 subunits is sufficient to induc

26 ellular levels of immunologically detectable G alpha q/G alpha 11 by 50% within 6 hr.

27 identified by immunoblot analysis as either G alpha q or G alpha 11.

28 yzed binding of GTP gamma S is selective for G alpha q, since we did not detect receptor-catalyzed ex

29 of G protein alpha subunits was specific for G alpha q/G alpha 11.

30 ressing G alpha q specifically in the heart (G alpha q-25) and nontransgenic siblings underwent micro

31 ction performance (compensated hypertrophy), G alpha q-25 left ventricles developed eccentric hypertr

32 diac gene expression observed at baseline in G alpha q-25 developed after aortic banding of nontransg

33 indings suggest that compensatory changes in G alpha q expression occur in mice with persistently alt

34 nearby residue in G alpha i to that found in G alpha q (K180P).

35 ivo and in vitro in myocytes after increased G alpha q activity, the trigger for pressure-overload hy

36 raises the possibility that agonist-induced G alpha q/G alpha 11 down-regulation participates in the

37 Ang II-induced G alpha q/G alpha 11 down-regulation was reversed by pre

38 Before aortic banding, isolated G alpha q-25 ventricular myocytes exhibited contractile

39 ellet was implanted subcutaneously into male G alpha q transgenic (Gq) mice.

40 Intrinsic cardiac myocyte G alpha q activation stimulates fetal gene expression an

41 o determine the effects of intrinsic myocyte G alpha q signaling on the left ventricular hypertrophic

42 Labeling of G alpha i but not G alpha q was antagonized by pertussis toxin.

43 s with the transition state mimetic forms of G alpha q, G alpha 12, and G alpha 13.

44 caused by cardiac-specific overexpression of G alpha q, i.p. ITPP increased exercise capacity, with a

45 reover, PHE stimulated the palmitoylation of G alpha q and G alpha o, and this response was blocked b

46 sulin-stimulated tyrosine phosphorylation of G alpha q/11 and IRS-1, as well as their association wit

47 ct interaction with, and transactivation of, G alpha q.

48 he ET-1-induced decrease in IRS-1 depends on G alpha q/11 and PI3-kinase.

49 ystem, while having no significant effect on G alpha q-stimulated PLC-beta 3 activity.

50 The effects of Ang II on G alpha q/G alpha 11 levels were inhibited when protein

51 e hemodynamic stress of pressure overload on G alpha q overexpression stimulates a maladaptive form o

52 irement for G alpha 13 but not G alpha 12 or G alpha q/11 in G2A-induced actin rearrangement.

53 ure overload, transgenic mice overexpressing G alpha q specifically in the heart (G alpha q-25) and n

54 able content of G-proteins (p21rhoA, p21ras, G alpha q/11, G alpha i3, and G beta) or protein kinase

55 anslocation via the heterotrimeric G protein G alpha q/11 and through PI3-kinase--mediated pathways i

56 of urea extracted membranes with a purified G alpha q showed that receptor-catalyzed binding of GTP

57 ssay was 60 nM, and the Km for squid retinal G alpha q was 90 nM.

58 ers of other G alpha subfamilies, G alpha s, G alpha q, and G alpha 12/13.

59 These data indicate that G alpha s, G alpha q/11, and G alpha i3 associate with Golgi membra

60 at GRP-R in these cells tonically stimulated G alpha q/11, resulting in increased phospholipase C act

61 of the Gq class of G protein alpha subunits (G alpha q/G alpha 11) in cultured rat vascular smooth mu

62 her heterotrimeric G-protein alpha-subunits (G alpha q/11, G alpha i1, and G alpha o) were not differ

63 them are activated to various extents by the G alpha q family of G proteins.

64 expression of mRNA and protein encoding the G alpha q subunit of G-protein that couples to 5-HT2A/2C

65 echanism of long term desensitization of the G alpha q/G alpha 11-mediated signaling system in VSMC.

66 We evaluated the role of the G alpha-q (Galphaq) subunit of heterotrimeric G proteins

67 GS18) is a GTPase-activating protein for the G-alpha-q and G-alpha-i subunits of heterotrimeric G-pro

68 Therefore G alpha q-stimulated cardiac hypertrophy is functionally

69 nstrate that GRPr can functionally couple to G alpha q but not to the pertussis toxin-sensitive G alp

70 A, and m1-muscarinic cholinergic) coupled to G alpha q and G alpha 13.

71 gh coupling of [3H]SCH23390 binding sites to G alpha q was unaltered in tissue taken from D1A mutant

72 y toward G alpha i compared with that toward G alpha q could be partially suppressed by mutation of t

73 ase in the total content of either trimeric (G alpha q/11, G alpha i3, and G beta) or monomeric (p21r

74 tive G alpha q mutant, but not the wild-type G alpha q, led to IRS-1 degradation and inhibited insuli

75 ted preferentially with tubulin-GDP, whereas G alpha q was transactivated by tubulin-GTP.

76 with G alpha 12 and G alpha 13 but also with G alpha q.

77 a 1b-, and alpha 1d-ARs were associated with G alpha q, alpha 1b-AR was also linked to G alpha o.