ライフサイエンスコーパス: Ala residue

1 the presence or absence of the N-terminal l-Ala residue.

2 or the presence or absence of the terminal l-Ala residue.

3 seven phosphorylation sites were replaced by Ala residues.

4 ither of these sites to non-phosphorylatable Ala residues.

5 ollowed by a repeating sequence of seven Pro/Ala residues.

6 762 sites (4Q4K FnbA) were substituted with Ala residues.

7 xposure relative to the spectra of the other Ala residues.

8 C(alpha)-H hydrogen-bond donation by subunit Ala residues.

9 nd the other with this residue surrounded by Ala residues.

10 appear to act as conformational hinges, with Ala residues.

11 -A) has an unusually large number of Pro and Ala residues (40% overall) and is 50% identical to FAP o

12 his protein's structure by mutating a small, Ala residue (A60) in its core to larger, hydrophobic sid

13 of several residues in the TSP1 peptide with Ala residues abolished or diminished the inhibitory acti

14 A-box or substitution of the GyrA-box with 7 Ala residues abolishes the ability of gyrase to wrap DNA

15 ive collagen binding trench of ACE N(2) with Ala residues affected collagen binding.

16 bic sequence composed of alternating Leu and Ala residues and flanked on both ends by two Lys) induce

17 residues were each mutated to both a Gly and Ala residue, and each mutant SHMT was purified and chara

18 occupancy of the heavy metal bound to the HQ-Ala residue, and the heavy metal provided excellent phas

19 idues of CtrA, particularly the terminal Ala-Ala residues, and another is located within the first 56

20 assembly samples, in which all Ile, Val, and Ala residues are uniformly labeled with 13C, are nearly

21 In this study, we have used Ala residues as probes for structural and dynamic change

22 AxG sequence, including a strongly conserved Ala residue at position 75 forming an interhelical kink.

23 The triple mutant containing Ala residues at 331, 332, and 333 was completely inactiv

24 Ala), significant activity is recovered when Ala residues at approximately parallel positions in heli

25 1-mer peptide (KAAKKAA)3, where three of the Ala residues at different positions have been replaced w

26 drophobic core is destabilized in the SCR by Ala residues at three consecutive d positions.

27 nt virus with a nonphosphorylatable alanine (Ala) residue at the site was markedly attenuated, wherea

28 ultaneous mutation of Thr 298 and Ser 305 to Ala residues attenuated the desensitization observed in

29 Reverse substitutions of the Ala residues by rhodopsin residues have been generated i

30 hat all mutant m2 receptors containing extra Ala residues C-terminal of Leu390 could activate the pro

31 Interestingly, introduction of extra Ala residues C-terminal of the AALS motif in the m3 musc

32 tion of Xrn2-Thr439 to a nonphosphorylatable Ala residue caused phenotypes consistent with inefficien

33 A human virus sequence with only Gly and Ala residues causes similar dysfunctions of eukaryotic a

34 ation of Thr(307), Thr(318), and Thr(319) to Ala residues dramatically reduces agonist-stimulated pho

35 nverted Cys-Pro motif had been replaced with Ala residues fails to bind hemin with high affinity.

36 similar to a phosphopeptide containing three Ala residues following Tyr(P) in binding to the Src SH2

37 he first inner loop, a substitution of three Ala residues for Met(128)-Arg(129)-Asn(130) abolished th

38 Substitutions of Ala residues for the conserved Asn, Asn193 or Asn402, in

39 tidase activity, that removes the terminal d-Ala residue from peptidoglycan.

40 s enzyme in both the removal of C-terminal d-Ala residues from stem peptides and the cleavage of cros

41 A sequence with only Gly and Ala residues (glycine-alanine repeat; GAr) encoded by th

42 istant enterococci in which the C-terminal D-Ala residue has been replaced by D-lactate.

43 ant m2 and m3 receptors that contained extra Ala residues immediately N-terminal of the VTIL and AALS

44 e severe effects than replacing Cys276 by an Ala residue in the active site of the enzyme, as encount

45 ution of Thr for an evolutionarily conserved Ala residue in the cytoplasmic S4-S5 linker of domain II

46 The replacement of Cys-199 by an Ala residue in the enzyme seems to increase the dissocia

47 otrophicus (Gd), which natively possesses an Ala residue in the position of the Ser ligand to the P-c

48 Replacing the five Phe with five Ala residues in MARCKS(151-175) decreases the binding to

49 SP-B(9-36), synthesized with (13)C=O-labeled Ala residues in positions 26, 28, 30, and 32, shifted th

50 residues (each contained 6 Leu, 3 Ile, and 7 Ala residues in the hydrophobic core) would affect helic

51 4') residues by 5-HT3B (-4'Gln, 0'Asp, and 4'Ala) residues increases gamma to 36.5 +/- 1.0 pS.

52 he residues or at side-chain methyl sites of Ala residues, indicate intermolecular (13)C-(13)C distan

53 Point mutagenesis of T257, S262, and T267 to Ala residues indicated that these sites are targets of p

54 d Thr ERK consensus phosphorylation sites to Ala residues inhibited the ability of the receptor to re

55 ulfide-bonded Cys residues was replaced with Ala residues, leaving four Cys residues that can form si

56 We also show that a conserved Ala residue limits thymine excision by hindering nucleot

57 all nonessential amino acids were altered to Ala residues, manifested subunit specificity similar to

58 o5 contained interpeptide bridges with one L-Ala residue only.

59 20), Cys(10)-Cys(30)) were mutated to Ser or Ala residues, overexpressed in E. coli, purified, and ch

60 e followed by a C-terminal Gly, Ser, or beta-Ala residue [poly-(gamma-Glu-Cys)n-Xaa].

61 The Ala residue promotes oxygenation on the reactive pentadi

62 Specifically, we substituted Val or Ala residues proximal to the binding position of the ade

63 ds (H47 and H67), and from nonligand Gln and Ala residues (Q48 and A66) present in the cluster-bindin

64 Mutation of Lys betaD3 to an Ala residue resulted in a modest reduction in binding af

65 n of the FR cavity V(H) Lys-19 residue by an Ala residue resulted in attenuated binding of the 421-43

66 harged (Glu, Lys) or small hydrophobic (Gly, Ala) residues resulted in complete loss of fusogenic act

67 that changes Ser421 to a nonphosphorylatable Ala residue (S421A).

68 The methyl groups of Thr and Ala residues show generalized order parameters ranging f

69 NA enters stalled ribosomes and transfers an Ala residue to the growing polypeptide chain.

70 Changing three Ala residues to canonical interface residues, A74L-A78V-

71 replaced with an aspartate (Asp) or alanine (Ala) residue to mimic the phosphorylated and nonphosphor

72 When Gly was replaced by Ala, the Ala residue was incorporated into a fully folded triple

73 tation, hydrogen abstraction, and the Gly or Ala residue we have identified.

74 carinic receptors in which one to four extra Ala residues were inserted into TM VI immediately after

75 membranes, whereas those with corresponding Ala residues were not.

76 Ala residues were substituted for the Arg/Lys residues (

77 ide chains and the conserved i + 4 and i + 8 Ala residues, where i indicates the positions of the Thr

78 76me1/me2) in vitro, determined by a Ser and Ala residue within motif IV, respectively, enabling DOT1