ライフサイエンスコーパス: G-alpha-i

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1 ut is unaffected in cells lacking G beta(1), G alpha i(2), or G alpha i(3).

2 [35S]G alpha i and [35S]G alpha q were immunoprecipitated fro

3 We previously identified a G alpha i homologue gna-1 in the filamentous fungus Neur

4 injection of G beta gamma, but not activated G alpha i, leads to the activation of MPF, entry into me

5 tion signals mediated by CCR7 and additional G alpha i-coupled receptors.

6 alpha q and G alpha o but not G alpha s and G alpha i precipitated specific alpha 1-AR binding sites

7 ase-activating protein for the G-alpha-q and G-alpha-i subunits of heterotrimeric G-proteins that tur

8 ha i GDP with PDE gamma is undetectable, but G alpha i GDP-A1F4- interacts weakly with PDE gamma (Kd

9 ng of Th2 cells into the lung is mediated by G alpha i-coupled chemoattractant receptors.

10 ect receptor-catalyzed exchange using either G alpha i/o or G alpha t.

11 t GIV/Girdin serves as a nonreceptor GEF for G alpha i through an evolutionarily conserved motif that

12 rtussis toxin, implicating a requirement for G alpha i--protein-linked signaling.

13 pressed by mutation of the nearby residue in G alpha i to that found in G alpha q (K180P).

14 pertussis toxin and genistein, inhibitors of G alpha i GTP-binding proteins and tyrosine kinases, res

15 evented these effects, whereas inhibitors of G alpha i or G beta gamma were without effect.

16 The interaction of G alpha i GDP with PDE gamma is undetectable, but G alph

17 Labeling of G alpha i but not G alpha q was antagonized by pertussis

18 in cells lacking G beta(1), G alpha i(2), or G alpha i(3).

19 ith a cortical Partner of Inscuteable (Pins)-G alpha i crescent to divide asymmetrically, but the lin

20 against a common sequence within G alpha s, G alpha i, and G alpha o showed no immunoreactivity to t

21 is a member of the pertussis toxin-sensitive G alpha i family.

22 a q but not to the pertussis toxin-sensitive G alpha i/o or retinal specific G alpha t.

23 eceptor (GPCR) Moody, the G protein subunits G alpha i and G alpha o, and the regulator of G protein

24 Using defined G alpha t/G alpha i chimeras, we have individuated the regions on

25 atment with pertussis toxin, suggesting that G alpha-i proteins are involved in TCA3 signaling of smo

26 LT receptor 1 antagonist CP 105,696, and the G alpha i inhibitor pertussis toxin.

27 pha i1 complex as a template, we modeled the G alpha i-GIV interface and identified the key residues

28 dy was undertaken to test whether one of the G alpha i proteins, G alpha i3, signals in the same path

29 to interact specifically with members of the G alpha i subfamily, G alpha i1, G alpha i2, G alpha i3,

30 blocked B cells and B cells treated with the G alpha i inhibitor, pertussis toxin, early after transf

31 or (GPCR) that coimmunoprecipitates with the G alpha i-subunit of heterotrimeric G-proteins from huma

32 ivation and chemotaxis that was sensitive to G alpha i and anti-receptor antibody inhibition.

33 erentially decreased the GAP activity toward G alpha i compared with that toward G alpha q could be p

34 ing the functional disruption of this unique G alpha i-GIV interface a promising target for therapy a

35 pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress comp

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