ライフサイエンスコーパス: trypsin treatment

1 ced by type B isolates remained active after trypsin treatment.

2 demonstrated by increased exposure following trypsin treatment.

3 time dependent and was destroyed by heat or trypsin treatment.

4 nfectivity of the particles before and after trypsin treatment.

5 s in the virion at various time intervals of trypsin treatment.

6 This effect is sensitive to trypsin treatment.

7 second developed slowly and was resistant to trypsin treatment.

8 cysteine is affected only twofold or less by trypsin treatment.

9 e protein that was protected from subsequent trypsin treatment.

10 the pyridoxal-P cofactor is eliminated after trypsin treatment.

11 soluble CD14 complexes was also inhibited by trypsin treatment.

12 ion of SARS-CoV could be strongly induced by trypsin treatment.

13 ide complex could be completely activated by trypsin treatment.

14 readily cleaved into its mature subunits by trypsin treatment.

15 was also directly measured, before and after trypsin treatment.

16 Moreover, in an in vitro digestive pepsin-trypsin treatment, 30% of quinoin is resistant to enzyma

17 em is supported by the inhibitory effects of trypsin treatment, 4,4'-diisothiocyanatostilbene-2,2'-di

18 However, prolonged trypsin treatment almost completely abolishes the infect

19 oma conditioned media were abolished by both trypsin treatment and heat inactivation, indicating the

20 In situ trypsin treatment and surface protein cross-linking show

21 osis and macrophage uptake were blocked with trypsin-treatment and soluble protein A.

22 to mice was evaluated with or without prior trypsin treatment, and monoclonal antibody neutralizatio

23 Based on results of CD spectroscopy, trypsin treatment, and MS, we propose a topological mode

24 ne type developed rapidly and was removed by trypsin treatment, and the second developed slowly and w

25 The factor was heat labile, was sensitive to trypsin treatment, and was retained after passage throug

26 horescence anisotropy changes observed after trypsin treatment are due to a rotational constraint cha

27 Trypsin treatment at 4 degrees C allowed for subsequent

28 e adhesive protein(s) on the IRBC surface to trypsin treatment at different stages of parasite develo

29 ]radioactivity of eEF1A could be released by trypsin treatment but not by carboxypeptidase Y or chymo

30 In contrast, trypsin treatment can both overcome ammonium chloride in

31 lly to mCD14 with a ratio of up to 15:1, and trypsin treatment decreased this uptake by more than hal

32 On the bilayer, trypsin treatment in the presence of urea resulted in th

33 t on APCs, but could be fully obliterated by trypsin treatment, indicating that a cell surface protei

34 Following additional trypsin treatment, infectivity was enhanced for both NTR

35 Trypsin treatment led to a stepwise removal of the prope

36 Trypsin treatment of [125I] DEEP-labeled membranes gener

37 Heat inactivation and trypsin treatment of cytosol, as well as addition of ATP

38 nantly resides on the surface of cells since trypsin treatment of HepG2 cells eliminated nearly 70% o

39 Trypsin treatment of immunoprecipitated phogrin generate

40 ide red cell ghosts cleaves at K743, as does trypsin treatment of inside-out vesicles (IOVs).

41 Mild trypsin treatment of intact mycoplasmas reduced binding

42 Consistent with their surface topology, mild trypsin treatment of LM protoplasts ablated T cell recog

43 Trypsin treatment of MDMs at 37 degrees C, which deplete

44 The C-terminal gamma10 fragment generated by trypsin treatment of membrane-bound and soluble CF1 are

45 gammma10) molecular weight were generated by trypsin treatment of membrane-bound CF1.

46 Photoaffinity labeling after trypsin treatment of membranes showed that the larger bu

47 de does not traffic to the surface membrane; trypsin treatment of microsomes containing this polypept

48 Similarly, trypsin treatment of monocytes inhibited IL-6 production

49 partial micrococcal nuclease digests and by trypsin treatment of nuclei, which results in mononucleo

50 Trypsin treatment of P41 cleaves the same bond in the C-

51 he approximately 29-kDa species generated by trypsin treatment of P41 is active, it is rapidly degrad

52 Exhaustive trypsin treatment of PAN generated five distinct fragmen

53 This conclusion was confirmed by trypsin treatment of permeabilized cells followed by Wes

54 y as well as immunoblot analysis showed that trypsin treatment of proteoliposomes containing His10K29

55 Trypsin treatment of Salmonella typhimurium EI yielded E

56 Trypsin treatment of STF abrogated their effects, while

57 the sigma1 cleavage product released during trypsin treatment of T3D virions to generate ISVPs and f

58 Trypsin treatment of the 46-kDa GPR zymogen (termed P46)

59 Trypsin treatment of the bacteria significantly reduced

60 pressing DeltaN-PSGL-1 bound P-selectin, and trypsin treatment of the cells generated NH(2)-terminal

61 d flagellins is dramatically reduced by mild trypsin treatment of the cells.

62 inhibited in the presence of heparin and by trypsin treatment of the cells.

63 Similarly, trypsin treatment of the nanosensor coated with cellular

64 This was accomplished by trypsin treatment of the purified reduced mucin subunit

65 affect viral entry, we tested the effect of trypsin treatment of the viral inoculum on growth of wt

66 Trypsin treatment of trifluoromethanesulfonic acid-treat

67 50-kDa protein, CMFR1, that is sensitive to trypsin treatment of whole cells.

68 The activity was destroyed by trypsin treatment or boiling of the extract, suggesting

69 reatment (overall mean, 40.6% inhibition) or trypsin treatment (overall mean, 83.3% inhibition).

70 Trypsin treatment produced a limit peptide (residues 1 t

71 ion in the presence of microsomal membranes, trypsin treatment removed 2 kDa from DBMsignal/PHMs whil

72 After intracellular trypsin treatment, salicylate reduced voltage-dependent

73 actor (the fungal metabolite brefeldin A and trypsin treatment) selectively inhibited the guanine nuc

74 Structural studies on the NTR TLPs after trypsin treatment showed that spike structure could be p

75 Trypsin treatment significantly reduced Pf-IRBC binding

76 incorporation by other dermal papilla cells; trypsin treatment significantly reduced the effect.

77 This activity of HDL was inhibited by trypsin treatment, suggesting that one or more protein c

78 with late trophozoites are more resistant to trypsin treatment than those containing early trophozoit

79 when DU4475 cells are subjected to the same trypsin treatment that is required for adherent cells, s

80 Upon removal by trypsin treatment, the surface-exposed population of PfE

81 The cell detachment ratio by trypsin treatment was slightly higher than that induced

82 Mild trypsin treatment was used to convert [Val217]phK2 to th

83 , as well as BPSA generated in vitro by mild trypsin-treatment were found to have a similar pattern o

84 Significantly, HD5 was resistant to trypsin treatment, whereas E14Q-HD5 was highly susceptib

85 his orientation was found to be unchanged by trypsin treatment, which cleaves band 3 between the inte

86 ptake after phospholamban phosphorylation or trypsin treatment, which cleaves the inhibitory cytoplas

87 Finally trypsin treatment, which preferentially cleaves the C-te