ライフサイエンスコーパス: adenyl

1 treatment, the nonhydrolyzable ATP analogue, adenyl 5'-(yl iminodiphosphate), does not enhance ADP tr

2 abrogated in vitro by ATP and the ATP analog adenyl-5'-yl imidodiphosphate.

3 of the nonhydrolyzable ATP analogue AMP-PNP (adenyl-5'-yl imidophosphate), the ectonucleotidase inhib

4 experimental data for the 3-atom-linked bis-adenyl and bis-naphthyl compounds are consistent with th

5 do-photoactive analogues of ATP, ADP, and 5'-adenyl-beta,gamma-imidodiphosphate (AMP-PNP) with the tw

6 mations are sterically accessible to the bis-adenyl compound than to the bis-naphthyl compound becaus

7 ound from stacking as extensively as the bis-adenyl compound.

8 atic interactions, why the 3-atom-linked bis-adenyl compounds should stack more than the bis-naphthyl

9 Adenyl cyclase activation resulted in diminished pyropho

10 gonist isoproterenol (by 42%), 10 muM of the adenyl cyclase activator forskolin (by 32%), and 500 muM

11 Treatment of aorta with the adenyl cyclase activator, forskolin, also demonstrated i

12 ed with protein kinase C (PKC) activator and adenyl cyclase activator.

13 se to catecholamine signals, when it reduced adenyl cyclase activity by upregulating the expression o

14 the cAMP-radioimmunoassay to the analysis of adenyl cyclase activity.

15 GTPase-activating protein that also inhibits adenyl cyclase activity.

16 ast, forskolin and NaF, direct activators of adenyl cyclase and Gs, respectively, elicited comparable

17 ptors (EP2, EP3, and EP4) that activate both adenyl cyclase and K(ATP) channels.

18 is pathway because it remains intact in Ras, adenyl cyclase and protein kinase A mutants.

19 rrhagic shock, whereas direct stimulation of adenyl cyclase by forskolin had no effect.

20 ling the toxin to translocate its N-terminal adenyl cyclase enzyme domain into the host cell cytoplas

21 -evoked NO release was also abolished by the adenyl cyclase inhibitor 2',5'-dideoxyadenosine, while d

22 ability to activate AMPK was blocked by the adenyl cyclase inhibitor 2'5'-dideoxyadenosine.

23 ated, but was significantly inhibited by the adenyl cyclase inhibitor MDL12330A or the PKA inhibitor

24 Synthesis of cAMP was inhibited with the adenyl cyclase inhibitor SQ22536.

25 ntly increased cAMP, which were prevented by adenyl cyclase inhibitor.

26 AMPK, which were prevented by inhibition of adenyl cyclase or MEK.

27 T7 receptors and couples to a stimulation of adenyl cyclase when expressed in COS-7 cells.

28 n and Paul Greengard of a dopamine-sensitive adenyl cyclase, accordingly, was a giant step forward.

29 c stimulation, it produces reduced levels of adenyl cyclase, and hence, attenuates the beta-adrenergi

30 well-defined site is clearly identified with adenyl cyclase, beta/gamma and regulator of G-protein si

31 rylation by forskolin, a potent activator of adenyl cyclase, decreases HDAC8's enzymatic activity.

32 ent studies show that edema factor, a potent adenyl cyclase, has the ability to make a substantial co

33 Forskolin, an activator of adenyl cyclase, increased COX-2 promoter activity via th

34 ance, including G-protein-coupled receptors, adenyl cyclase, protein kinase A and cAMP response eleme

35 h encode the Ras GDP/GTP exchange factor and adenyl cyclase, respectively, and MDS3, which encodes a

36 ation is inhibited by cAMP analogues and the adenyl cyclase-stimulating agent forskolin.

37 al signaling pathway involving Galpha(s) and adenyl cyclase.

38 but not to forskolin, a direct activator of adenyl cyclase.

39 SpoIIE and a 300-residue domain within yeast adenyl cyclase.

40 ocyanobilin via their cGMP phosphodiesterase/adenyl cyclase/FhlA (GAF) domains and then assume the ph

41 r linkages within the cGMP phosphodiesterase/adenyl cyclase/FhlA domain.

42 conserved within the cGMP phosphodiesterase/adenyl cyclase/FhlA domain.

43 g of the Te-PixJ GAF (cGMP phosphodiesterase/adenyl cyclase/FhlA) domain assembled with phycocyanobil

44 (Per-ARNT-Sim), GAF (cGMP phosphodiesterase/adenyl cyclase/FhlA), and PHY (phytochrome) domains to a

45 NG oligomers is 2:1, as seen in thymidyl and adenyl DNA triplexes.

46 Binding of thymidyl DNA oligomers to adenyl DNG oligomers is 2:1, as seen in thymidyl and ade

47 No binding of adenyl DNG with octameric cytidyl DNA was observed, indi

48 It has been argued that the stacking of adenyl groups in water must be driven primarily by elect

49 based upon NMR data showing stacking for two adenyl groups joined by a 3-atom linker but not for two

50 roups tend to lie further apart than stacked adenyl groups, based upon both quantum calculations and

51 e the linker is attached to the sides of the adenyl groups, but to the ends of the naphthyl groups.

52 ne-5'-O-(3-thiotriphosphate) (ATPgammaS) and adenyl-imidodiphosphate, each stabilized the primer reco

53 ce of adenosine 5'-O-(3-thiotriphosphate) or adenyl-imidodiphosphate.

54 iversal methyl donor and gets converted to S-adenyl-l-homocysteine (SAH), an endogenous competitive i

55 S-Adenyl-l-methionine (SAM) is a universal methyl donor an

56 the minor conformation, but suggest that the adenyl moiety in the modified nucleoti111S,R, S,RA6 adop

57 In Y78F mutant complexes, adenyl nucleotide glycosidic torsion angles were 55 +/-

58 ting not only signals from the energy state (adenyl-nucleotide binding) and the carbon supply via cAM

59 Thus, the adenyl nucleotides bind similarly for both the wild type

60 For adenyl nucleotides in wild type complexes, all glycosidi

61 sphates over nucleotide diphosphates and for adenyl nucleotides over the corresponding guanyl ones wa

62 However, for K14M with adenyl nucleotides, the glycosidic torsion angle was 30

63 For R41M with adenyl nucleotides, the glycosidic torsion angle, chi, w

64 The results indicate that bound adenyl-nucleotides have significantly different conforma

65 of ATP release and the relative abundance of adenyl purines and, hence, to define their biological fu

66 1,N(6)-ethenoadenine derivatives to measure adenyl purines in ASL.

67 considered to be depurination of a specific adenyl residue of ribosomal RNA, resulting in inhibition

68 articularly for genes of phosphorylation and adenyl ribonucleotide binding, and proteins located in n

69 rating cell nuclear antigen and cleaved poly(adenyl ribose) polymerase, a marker of apoptosis.

70 rating cell nuclear antigen and cleaved poly(adenyl ribose) polymerase.

71 N(6)-adenyl)styrene oxide and (S)-beta-(N(6)-adenyl)styrene oxide adducts at position X(6) in d(CGGAC

72 The (S)-alpha-(N6-adenyl)styrene oxide adducts at positions X6 in d(CGGACX

73 Conformational studies of R- and S-alpha-(N6-adenyl)styrene oxide adducts mismatched with deoxycytosi

74 Conformations of (R)-beta-(N(6)-adenyl)styrene oxide and (S)-beta-(N(6)-adenyl)styrene o

75 confirmed the presence of the aminoglycoside adenyl transferase (aadA) gene, conferring St Spc resist

76 tRNA(Trp) and catalyzes the formation of 5' adenyl-Trp and tRNA(Trp), with approximately five times

77 ersion that abolishes secretion, uridyl 9 to adenyl (U9A), is a synonymous codon 3 mutation that reta