ライフサイエンスコーパス: Met residue

1 ents (the S6 bundle crossing) at a conserved Met residue.

2 O2, the smallest peroxide, to oxidise buried Met residues.

3 :60) resulted in oxidation of six identified Met residues.

4 molecules of heme axially coordinated by two Met residues.

5 Ps) due to frequent initiation on downstream Met residues.

6 l, although it specifically targets oxidized Met residues.

7 anomalous dispersion (MAD) scattering by Se-Met residues.

8 its catalase contains oxidizable methionine (Met) residues.

9 Oxidation of all nine CaM Met residues abolished functional interactions of CaM wi

10 on the CcPK2 mutant template to test if the Met residues also contribute to the stabilization of the

11 dduct at Cys-109, partial oxidation at all 7 Met residues, and evidence for two disulfide bonds.

12 cterial oxidant produced by neutrophils, and Met residues are considered primary amino acid targets o

13 As Met residues are known to protect proteins against ROS-m

14 Peptidyl Met residues are readily oxidized by reactive oxygen spe

15 tability of the Trp radical decreases as the Met residues are removed from the proximal cavity.

16 l caused oxidation of specific MS-identified Met residues, as well as structural changes and activity

17 on in the core, involving a highly conserved Met residue at position 67, appeared intolerant to subst

18 whereas Imp2p prefers substrates having the Met residue at the +1 position.

19 o acid modifications, such as three oxidized Met residues at positions 79, 141 and 187 and one deamid

20 gle-nucleotide polymorphism substitutions of Met residues by Thr in cancer-related proteins.

21 The oxidation of Met residue causes loss of bioactivities, strengthening

22 cerevisiae, we found that the Nt-acetylated Met residue could act as a degradation signal (degron),

23 These results thus identify Met residues critical for the productive association of

24 ntricate network of interactions involving c-Met residues documented previously to cause dysregulatio

25 se of excess methionine (Met) to protect mAb met residues from AAPH oxidation did not substantially a

26 excess free met did effectively protect mAb met residues from oxidation, and that AAPH-oxidized mAb

27 for proteins whose initiator methionine ((i)Met) residues have been removed.

28 However, the presence of the Met residue in the apolar interface of the tetramer mark

29 action of peroxidized lipids, the N-terminal Met residues in alphaS (Met1 and Met5) rapidly oxidize w

30 he basis of the hypothesis that oxidation of Met residues in calmodulin-binding domains inhibits bind

31 tivation gate, replacement of the homologous Met residues in human Slo2.1 or Slo2.2 with the negative

32 in, and mutations or deletions of His and/or Met residues in its sequence inhibit dephosphorylation o

33 version to peroxynitrite, that intracellular Met residues in proteins constitute a critical target fo

34 Met residues in proteins were fully oxidized using hydro

35 ed sample, in contrast, four solvent-exposed Met residues in the Fc portion were completely oxidized.

36 ng but greatly decreased the modification of met residues in the mAb.

37 tuted 27 hydrophobic Phe, Ile, Leu, Val, and Met residues in the regulatory domain of the fluorescent

38 Mutation of the conserved Met residues in the S6 segments to the negatively-charge

39 d previously that mutating conserved Phe and Met residues in the TA of ADGRL3-C-terminal fragment (CT

40 This peptide contains a methionine (Met) residue in the C-terminal domain, which is importan

41 e hydrogen peroxide oxidation of methionine (Met) residues in proteins to make DeltaG(f) value measur

42 Accordingly, Met-S=O formation of Met residues, including Met 374 in the active site of ty

43 Incomplete CaM oxidation, affecting 5-8 Met residues, increased the CaM concentration required t

44 s was accomplished be selectively converting Met residues into Leu, prior to Met oxidation.

45 However, the carbamidomethylation of Met residues leads to sulfonium ether formation, and the

46 The acetylated N-terminal Met residue of Hcn1 is enclosed within a chamber created

47 us, in complex with Cdc16/Cut9, the N-acetyl-Met residue of Hcn1, a putative degron for the Doa10 E3

48 roup is normally removed from the N-terminal Met residue of the peptide by peptide deformylase (PDF).

49 t exposure to ROS converted four out of nine Met residues of RecA to methionine sulfoxide.

50 The retained N-terminal methionine (Met) residue of a nascent protein is often N-terminally

51 peroxide, to oxidise only solvent accessible Met residues or H2O2, the smallest peroxide, to oxidise

52 The same HOCl-sensitive Met residue oxidation targets in catalase were detected

53 nd Ala), basic (Arg), and sulfur-containing (Met) residues rapidly, while P1 Asp or Gly were cleaved

54 reactive lipid hydroxide, whereas C-terminal Met residues remain unaffected.

55 hing harmful oxidants through its recyclable Met residues, resulting in oxidant protection to the bac

56 mRNA, likely from downstream initiation on a Met residue that comprises the P1 position of NS1-ARF2(1

57 ncerning Nature's selection of an oxidizable Met residue to facilitate C-H oxygenation.

58 There are 42 amino acids from the start Met residue to the beginning of the first 'VERL repeat'.

59 Mutating individual CaM Met residues to Gln demonstrated that Met-109 was requir

60 Mutations of 4 Met residues to Ile or two His-His pairs to Ala-Gly decr

61 esidues, in addition to causing oxidation of Met residues to Met-sulfoxide.

62 er insights into the susceptibility of CaM's Met residues to oxidation and the resulting structural e

63 urin was used to study the susceptibility of Met residues to oxidation by H 2O 2.

64 alian cells, approximately 1% of methionine (Met) residues used in protein synthesis are aminoacylate

65 Oxidation at Tyr, Trp, and Met residues was promoted by dissolved O(2).

66 These Met residues were also oxidized in ADAMTS13 exposed to a

67 without enzyme activity but that retain all Met residues were created.

68 nitrite and GSNO kill bacteria by oxidizing Met residues when these RNI cannot themselves oxidize Me

69 ually substituted 27 Phe, Ile, Leu, Val, and Met residues with polar Gln to examine the role of hydro

70 foxide were detected for the two susceptible Met residues with this new method compared to a typical