ライフサイエンスコーパス: hematin

1 to sites on the fastest growing face of beta-hematin.

2 quine and quinidine on the formation of beta-hematin.

3 bited a novel high-affinity binding site for hematin.

4 assical GST substrates but effectively binds hematin.

5 sis, hypertransfusion, and infusions of i.v. hematin.

6 anism regulates the access of chloroquine to hematin.

7 crystallites are identical to synthetic beta-hematin.

8 e products formed from 15R- and 15S-HPETE by hematin (a nonenzymatic reaction), by liver microsomes i

9 ated whole blood, moderate concentrations of hematin activate the alternative pathway of complement a

10 t chloroquine inhibits the polymerization of hematin, allowing this toxic hemoglobin metabolite to ac

11 sary to wash the pellet, which contains beta-hematin and heme aggregates, sequentially with Tris/SDS

12 ent on the saturable binding of the drugs to hematin and that the inhibition of hematin polymerizatio

13 g resulted in decreased final yields of beta-hematin, and an irreversible drug-induced precipitation

14 ation of sequence-specific DNA by exploiting hematin as biomimetic catalyst toward in situ metallizat

15 Under optimal conditions, the hematin-based electrochemical DNA biosensor presented a

16 Therefore, the hematin-based signal amplification approach has great po

17 Compared to CQ, hematin binding affinity of 1 decreased 6.4-fold, and th

18 nding, 13 CQ analogues were chosen and their hematin binding affinity, inhibition of hematin polymeri

19 support the hypothesis that chloroquine (CQ)-hematin binding in the parasite food vacuole leads to in

20 understand the structural specificity of CQ-hematin binding, 13 CQ analogues were chosen and their h

21 nes also form various complexes with soluble hematin, but complexation is insufficient to suppress he

22 The chemistry relies on the hematin-catalyzed oxidation of nonfluorescent thiamine t

23 embrane diffusion scrubber (DS) is used with hematin-catalyzed oxidation of thiamine to thiochrome fo

24 ential that are difficult or impossible with hematin-containing digestive vacuoles from P. falciparum

25 ow that quinoline antimalarials inhibit beta-hematin crystal surfaces by three distinct modes of acti

26 irst evidence of the molecular mechanisms of hematin crystallization and inhibition by chloroquine, a

27 her studies reveal that chloroquine inhibits hematin crystallization by binding to molecularly flat {

28 Hematin crystallization is the primary mechanism of heme

29 y, divergent hypotheses on the inhibition of hematin crystallization posit that drugs act either by t

30 stive vacuole through polymerization of beta-hematin dimers.

31 ows that the external morphology of the beta-hematin DMSO solvate crystals is almost indistinguishabl

32 mmon with chloroquine the inhibition of beta-hematin formation in a cell-free system.

33 ies bound to hematin monomer, inhibited beta-hematin formation in vitro, delayed intraerythrocytic pa

34 s, which are known to initiate/catalyze beta-hematin formation in vitro.

35 The decreased rate of beta-hematin formation observed at low concentrations of both

36 No beta-hematin formation occurred in the absence of a catalytic

37 rate quantification of de novo hemozoin/beta-hematin formation was verified experimentally.

38 how only weak activity as inhibitors of beta-hematin formation, and their activities are only weakly

39 drug chloroquine, a known inhibitor of beta-hematin formation.

40 a spectrophotometric assay for in vitro beta-hematin formation.

41 a widely accepted protocol for in vitro beta-hematin formation.

42 nteractions with Fe(III)PPIX, inhibited beta-hematin formation.

43 gregates and accurate quantification of beta-hematin formed during the assay.

44 n and characterization of PfCRT-transformed, hematin-free vesicles from D. discoideum cells.

45 This is the first case of the use of hematin given post-OLT to help achieve and maintain remi

46 ophysiology, fundamental questions regarding hematin growth and inhibition remain.

47 tes, lipopolysaccharides, and synthetic beta-hematin had minimal effect.

48 min was used to synthesize the crystal, beta-hematin had no inflammatory activity.

49 ted malarial trophozoites and synthetic beta-hematin have been measured; both materials correspond to

50 for their effects on the inhibition of beta-hematin (hemozoin) formation, and the results were compa

51 ials inhibit crystallization by sequestering hematin in the solution, or by blocking surface sites cr

52 After normalization of liver tests, the hematin infusions have been given intermittently, are we

53 or hematologists because they administer the hematin infusions to treat the acute attacks in patients

54 er lesions, which regressed with glucose and hematin infusions.

55 Well-developed SAR models exist for beta-hematin inhibition, parasite activity, and cellular mech

56 Evidently, the CQ-hematin interaction is largely a function of its pyridin

57 EXP1 efficiently degrades cytotoxic hematin, is potently inhibited by artesunate, and is ass

58 g suggests that the high-affinity binding of hematin may represent a parasite adaptation to blood or

59 Next, the attached hematin molecules acted as catalyst in accelerating the

60 After that, hematin molecules were introduced to the hybridized PNA/

61 Both series bound to hematin monomer, inhibited beta-hematin formation in vit

62 measure any significant interaction between hematin mu-oxo dimer and 11, the 6-chloro analogue of CQ

63 e out-of-plane pi-electron density in CQ and hematin mu-oxo dimer at the points of intermolecular con

64 merization IC(50) values were normalized for hematin mu-oxo dimer binding affinities, adding further

65 vorable pi-pi interaction observed in the CQ-hematin mu-oxo dimer complex derives from a favorable al

66 ues suggests that other properties of the CQ-hematin mu-oxo dimer complex, rather than its associatio

67 tural determinant in its binding affinity to hematin mu-oxo dimer.

68 like CQ, these analogues bind to two or more hematin mu-oxo dimers in a cofacial pi-pi sandwich-type

69 reaction of linoleate 10S-hydroperoxide with hematin or ferrous ions.

70 s act either by the sequestration of soluble hematin or their interaction with crystal surfaces.

71 pheromonal compounds include organic acids, hematin, or ecdysteroids.

72 hematin polymerization and parasite death by hematin poisoning.

73 s a modest correlation between inhibition of hematin polymerization and inhibition of parasite growth

74 correlation between potency of inhibition of hematin polymerization and inhibition of parasite growth

75 parasite food vacuole leads to inhibition of hematin polymerization and parasite death by hematin poi

76 ring are required for activity against both hematin polymerization and parasite growth and that chlo

77 13, the lack of correlation between K(a) and hematin polymerization IC(50) values suggests that other

78 ation and inhibition of parasite growth when hematin polymerization IC(50) values were normalized for

79 drugs to hematin and that the inhibition of hematin polymerization may be secondary to this binding.

80 Bisquinolines 1-10 were potent inhibitors of hematin polymerization with IC50 values falling in the n

81 heir hematin binding affinity, inhibition of hematin polymerization, and inhibition of parasite growt

82 tant alone, play a role in the inhibition of hematin polymerization.

83 Hz; malarial pigment) and synthetic Hz (beta-hematin) promote a similar pattern of beta-chemokine gen

84 Thus, the reaction mediated by hematin promotes opsonization and possible clearance of

85 due solely to the binding of chloroquine to hematin rather than active uptake: using Ro 40-4388, a p

86 cuole to alter the binding of chloroquine to hematin rather than changing the active transport of chl

87 In the hematin reaction, the major products are four epoxy alco

88 ggest a key role for pH-dependent changes in hematin receptor concentration in the P. falciparum CQR

89 Furthermore, hematin-reconstituted PGHS-1, which was rapidly inhibite

90 of hemoglobin digestion and, by implication, hematin release, we demonstrate a concentration-dependen

91 ent, which is approximately 10(4)x less than hematin's physiological concentration.

92 All inhibited both beta-hematin (synthetic hemozoin) formation and hemozoin form

93 different assay protocols for in vitro beta-hematin (synthetic identical to hemozoin) formation by t

94 n nucleation in vivo, and nucleation of beta-hematin, the synthetic analogue of hemozoin, was consist

95 chloroquine flux or reduced drug binding to hematin through an effect on DV pH.

96 neration of enzyme activity, but addition of hematin to the inhibited apoenzyme led to spontaneous re

97 "Synthetic" HZ (beta-hematin), typically generated from partially purified ex

98 The high-affinity binding site for hematin was not present in the GST showing the most iden

99 Single crystals of solvated beta-hematin were grown from a DMSO solution containing the a

100 te breakdown products such as hemoglobin and hematin, which have inflammatory properties.