ライフサイエンスコーパス: ABH

1 ABH binds with high affinity to phosphatidylinositol-3-p

2 ABH(O) blood group polymorphisms are based on well-known

3 protein, with specificity for type 1 and 11 ABH blood group epitopes and polylactosamine glycan cont

4 Out of 397 ABHs, 55.7% evolved to a PBH.

5 However, at pH 9.5, ABH and BEC are slow-binding inhibitors of the enzyme wi

6 inhibitor 2(S)-amino-6-boronohexanoic acid (ABH) (K(d) = 11 microM).

7 analogues 2(S)-amino-6-boronohexanoic acid (ABH) and S-(2-boronoethyl)-L-cysteine (BEC), which are k

8 e analogue 2(S)-amino-6-boronohexanoic acid (ABH) binds as a tetrahedral boronate anion to Mn(2+)(2),

9 inhibitors 2(S)-amino-6-boronohexanoic acid (ABH, Kd = 5 nM) and S-(2-boronoethyl)-l-cysteine (BEC, K

10 e analogue 2(S)-amino-6-boronohexanoic acid (ABH, pH 7.0) and the catalytic product L-Orn (pH 7.0) de

11 A BH was considered as acute (ABH) when it occurred coincidently with the presence of

12 PDs were associated with subsequent ABD and ABH loss (P <0.05 for each).

13 pths were associated with subsequent ABD and ABH loss (p<0.05 for each).

14 ne PD was associated with subsequent ABD and ABH loss.

15 ne PD was associated with subsequent ABD and ABH loss.

16 lamed eyes of B10R III, C57BL/6, BALB/c, and ABH Biozii mice were immunostained for APC markers (33D1

17 anges did not predict 2-year ABH changes and ABH/ABD changes, respectively.

18 ges did not predict two-year ABH changes and ABH/ABD changes, respectively.

19 nd competitive binding studies of CvGal1 and ABH-specific monoclonal antibodies with intact and degly

20 l therapy against liver-stage infection, and ABH may serve as a lead for the development of inhibitor

21 Oligosaccharides containing the Lewis and ABH antigenic epitopes were involved in binding.

22 ut strong selection for retention of RID and ABH suggests these two domains may primarily function by

23 ells of heart and spleen, only type II-based ABH antigens were expressed; type III/IV structures were

24 Type II-based ABH were expressed on erythrocytes of all blood groups.

25 PD were positively associated with baseline ABH loss (P <0.0001), and baseline PDs were associated w

26 PD were positively associated with baseline ABH loss (p<0.0001) and baseline probing depths were ass

27 Because ABH antigen subtypes are expressed differently in variou

28 Because ABH binds as an analogue of the tetrahedral intermediate

29 s (NLVs) have various capacities for binding ABH histo-blood group antigens, suggesting that differen

30 n by sensitization to myelin antigens Biozzi ABH mice also develop spasticity and tremor.

31 At pH 7.5, both ABH and BEC are classical, competitive inhibitors of hum

32 trate the inhibition of arginase activity by ABH in human and murine myeloid cells.

33 ously unstudied alpha-beta hydrolase domain (ABH) is shown here to activate CDC42, although the effec

34 ts of anti-IL-17A in a chronic relapsing EAE ABH mouse model using conventional scoring, quantitative

35 istic, with 5% of A1 donors typing as either ABH high- or low-expressers.

36 ve experimental autoimmune encephalomyelitis ABH mouse model of multiple sclerosis using conventional

37 Platelets express ABH antigens, which can adversely effect platelet transf

38 protein that mediates binding to fucosylated ABH antigens of the ABO blood group.

39 idues as critical for binding to fucosylated ABH antigens.

40 Blood group ABH(O) carbohydrate antigens are carried by precursor st

41 bone density (ABD) and alveolar bone height (ABH) measurements.

42 bone density (ABD) and alveolar bone height (ABH) measurements.

43 Angina bullosa hemorrhagica (ABH) describes benign subepithelial oral blood blisters

44 sis of beta-alkyl N-aryl aza Baylis-Hillman (ABH) adducts is reported.

45 leton, the function of alpha-beta hydrolase (ABH) remained elusive.

46 resolution structure of the human arginase I-ABH complex yields an unprecedented view of the binuclea

47 e phase errors in genotypic data that are in ABH format.

48 qualitative and quantitative differences in ABH antigen expression between erythrocytes and vascular

49 o be used to correct linkage phase errors in ABH formatted datasets.

50 latelet transfusion recovery and survival in ABH-incompatible recipients.

51 zed against chemically synthesized type I-IV ABH and related glycans.

52 ons do not affect the binding of monofucosyl ABH HBGAs but that they can modulate the binding strengt

53 Interestingly, antibodies to other non-ABH glycans, such as the alpha-Gal antigen, also correla

54 he host immune system of exposure to nonself ABH antigens during early life in human heart versus por

55 , IgG, and IgA isotype antibodies to nonself ABH subtypes were detected in control participants and r

56 allyl esters and carbonyl compounds to novel ABH adducts.

57 In a search for the molecular basis of ABH status of tumors as correlated with malignancy, we s

58 ng to P. marinus trophozoites, no binding of ABH blood group antibodies was observed.

59 es encoding and regulating the expression of ABH and Lewis antigens in bodily secretions particularly

60 It is widely thought that expression of ABH antigens on platelets is insufficient to materially

61 Expression of ABH in vivo reduces intracellular PtdIns3P levels and it

62 the clinical and histopathologic features of ABH which appeared after routine scaling and root planin

63 The odds of ABH loss were higher among sites with concurrent 1-year

64 The odds of ABH loss were higher among sites with concurrent one-yea

65 Little is known about the pathogenesis of ABH, although most cases have been associated with mild

66 is the first report highlighting the role of ABH in inhibiting autophagy and endosomal trafficking in

67 ficient to materially affect the survival of ABH-incompatible platelets in transfusion recipients, bu

68 ype II and/or B subtype II antigens-the only ABH antigen subtypes expressed in heart tissue-were abse

69 Among A1 donors, platelet ABH varied significantly between donors (0%-87%).

70 wever, was minimal, suggesting that platelet ABH expression is a stable, donor-specific characteristi

71 Unlike RBCs, ABH expression on platelets may be determined primarily

72 ns to the underlying H(O) structure, we show ABH antigens stabilize sialylated glycan clusters on ery

73 (HV) virus-like particles (VLPs) to specific ABH histo-blood group antigens was investigated by using

74 her show that by stabilizing such structures ABH antigens can also modulate sialic acid-mediated inte

75 We studied ABH expression in 166 group A apheresis platelet donors

76 This study demonstrates that ABH is an esterase/lipase with catalytic Ser-His-Asp tri

77 We show in this study that ABH antigens found on human erythrocytes modulate the sp

78 ha(1,2)fucosyltransferase gene (FUT2) in the ABH histo-blood group family and did not express the H t

79 ; induction and control of spasticity in the ABH mouse model of multiple sclerosis; conditional delet

80 rcome the substrate scope limitations of the ABH reaction, which converts allyl esters and carbonyl c

81 Thus, ABH antigens can noncovalently alter the presentation of

82 exhibit different patterns of attachment to ABH histo-blood group antigens, which are carbohydrate e

83 force, direct binding of lethal pathogens to ABH antigens has not been reported.

84 study comparing specific donor factors with ABH expression on platelet membranes and glycoconjugates

85 he P domain structure of a 2004 variant with ABH and secretor Lewis HBGAs and compared it with the pr

86 e able to block the interaction of VLPs with ABH histo-blood group antigens (HBGA), suggesting that m

87 lative CAL/PD changes did not predict 2-year ABH changes and ABH/ABD changes, respectively.

88 ear RCAL/PD changes did not predict two-year ABH changes and ABH/ABD changes, respectively.