ライフサイエンスコーパス: Galpha11

1 gnals through the G-protein subunit alpha11 (Galpha11).

2 at was derived from mice lacking Galphaq and Galpha11.

3 those directed against Galphao, Galphaq and Galpha11.

4 wild type and four lines of mutant mice: 1) Galpha11-/-, 2) Galpha11-/-/Galpha14-/-, 3) Galpha14-/-/

5 ly reduced DOI-stimulated phosphorylation of Galpha11 and DOI-induced desensitization of 5-HT2A recep

6 Galphai2, Galphai3, Galphaz) as well as for Galpha11 and Galphas.

7 at RGS3 bound to aluminum fluoride-activated Galpha11 and to a lesser extent to Galphai3 and that thi

8 retion was defective in both EC-Galphaq(-/-);Galpha11(-/-) and Galpha12(-/-) mice.

9 hree of the four Gq class subunits, Galphaq, Galpha11, and Galpha14 but not Galpha15.

10 We conclude that Galphaq, Galpha11, and Galpha14 promiscuously couple several rece

11 PLC beta3 can be activated by Galphaq, Galpha11, and Galpha16 in the cotransfection assay.

12 By contrast, anti-Galphaq/Galpha11 antibodies greatly inhibited ICl(Ca), but did n

13 of two G protein alpha subunits, Galphaq and Galpha11, differ from those of other alpha subunits in t

14 in the G protein alpha subunits Galphaq and Galpha11 (encoded by GNAQ and GNA11, respectively) occur

15 We also postulated that mutations effecting Galpha11 gain of function, like the mutations effecting

16 RGS3 with a constitutively active mutant of Galpha11 (Galpha11-QL) resulted in the binding of RGS3,

17 G12 class of G proteins, including Galphaq, Galpha11, Galpha14, Galpha16, Galpha12, and Galpha13, ca

18 our lines of mutant mice: 1) Galpha11-/-, 2) Galpha11-/-/Galpha14-/-, 3) Galpha14-/-/Galpha15-/-, and

19 i3, Galphaz) or unrelated (Galphas, Galphaq, Galpha11, Galpha16, Galpha12, Galpha13) Galpha subunits.

20 and the G protein alpha subunits Galphaq and Galpha11 (Galphaq/11) transmit mechanical and chemical s

21 rotein kinase C beta, Fyn, CD22, Galphaq, or Galpha11 had no detectable effect on the function of Btk

22 /-) double-knockout mice (which express only Galpha11 in most hematopoietic cells), and Galpha11(-/-)

23 s GTPase-activating proteins for Galphaq and Galpha11 in P2Y1-R-containing vesicles.

24 s effecting Galpha11 loss of function, since Galpha11 is involved in calcium-sensing receptor signali

25 pe 2 had an in-frame deletion of a conserved Galpha11 isoleucine (Ile200del), and one of the nine unr

26 ed that type 2 is due to mutations effecting Galpha11 loss of function, since Galpha11 is involved in

27 2+) i responses of FHH2- and ADH2-associated Galpha11 loss- and gain-of-function mutations, respectiv

28 y Galpha11 in most hematopoietic cells), and Galpha11(-/-) mice, suggesting functional redundancy in

29 d the effect of NPS-2143 on a uveal melanoma Galpha11 mutant.

30 lial hypocalciuric hypercalcemia type 2, and Galpha11 mutants with gain of function cause a clinical

31 Galpha11 mutants with loss of function cause familial hy

32 ers and tumorigenesis; and that ADH2-causing Galpha11 mutations induce non-constitutive alterations i

33 type 2 (ADH2), respectively, whereas somatic Galpha11 mutations mediate uveal melanoma development by

34 d the influence of germline gain-of-function Galpha11 mutations on MAPK signaling by measuring ERK ph

35 ADH2-causing Galpha11 mutations were demonstrated not to be constitut

36 tions associated with FHH2- and ADH2-causing Galpha11 mutations, and evaluated the influence of germl

37 disturbances caused by germline and somatic Galpha11 mutations, which respectively lead to calcium d

38 in the GnRH neurons of global Gna11 (encodes Galpha11)-null mice by crossing Gnrh-Cre and Gnaq(fl/fl)

39 These data suggest that phosphorylation of Galpha11 protein by PKC and CaMK contributes to agonist-

40 We were unable to detect Galphaq or Galpha11 protein coupling to homomers or heteromers of D

41 to modulate abnormalities of the downstream Galpha11 protein is unknown.

42 we studied the effects of GNA11 mutations on Galpha11 protein structure and calcium-sensing receptor

43 WT and mutant Galpha11 proteins causing FHH2, ADH2 or uveal melanoma w

44 Signaling from Galpha11/q-linked GPCRs to Rho was not impaired in mouse

45 embrane fraction and in its interaction with Galpha11-QL in vitro without any stimuli.

46 a constitutively active mutant of Galpha11 (Galpha11-QL) resulted in the binding of RGS3, but not of

47 Expression of Galpha11 S154D, a phosphorylation mimic, reduced DOI-sti

48 in dependent kinase (CaMK) consensus site in Galpha11 significantly reduced DOI-stimulated phosphoryl

49 Interfering with Galphaq or Galpha11 using dominant negative cDNA constructs or siRN

50 of-function mutations of G-protein alpha-11 (Galpha11), which couples the calcium-sensing receptor (C