ライフサイエンスコーパス: trypsin treatment

1 demonstrated by increased exposure following trypsin treatment.

2 This effect is sensitive to 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 second developed slowly and was resistant to trypsin treatment.

7 ion of SARS-CoV could be strongly induced by 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 readily cleaved into its mature subunits by trypsin treatment.

12 soluble CD14 complexes was also inhibited by trypsin treatment.

13 ide complex could be completely activated by trypsin treatment.

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

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

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

17 However, prolonged trypsin treatment almost completely abolishes the infect

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

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

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

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

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

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

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

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

26 Trypsin treatment at 4 degrees C allowed for subsequent

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

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

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

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

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

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

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

34 Trypsin treatment led to a stepwise removal of the prope

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

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

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

38 Trypsin treatment of immunoprecipitated phogrin generate

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

40 Mild trypsin treatment of intact mycoplasmas reduced binding

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

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

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

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

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

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

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

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

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

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

51 Exhaustive trypsin treatment of PAN generated five distinct fragmen

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

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

54 Trypsin treatment of Salmonella typhimurium EI yielded E

55 Trypsin treatment of STF abrogated their effects, while

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

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

58 Trypsin treatment of the bacteria significantly reduced

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

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

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

62 Similarly, trypsin treatment of the nanosensor coated with cellular

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

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

65 Trypsin treatment of trifluoromethanesulfonic acid-treat

66 50-kDa protein, CMFR1, that is sensitive to trypsin treatment of whole cells.

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

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

69 Trypsin treatment produced a limit peptide (residues 1 t

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

71 After intracellular trypsin treatment, salicylate reduced voltage-dependent

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

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

74 Trypsin treatment significantly reduced Pf-IRBC binding

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

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

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

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

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

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

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

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

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

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