ライフサイエンスコーパス: NADase

1 NADase (SPN) and streptolysin O (SLO) are two toxins tha

2 NADase purified from GAS altered neutrophil-directed mig

3 These findings suggest that SPN has a NADase-independent function and prompt a reevaluation of

4 keratinocytes to wild-type GAS, but not to a NADase-deficient mutant strain, resulted in profound dep

5 nsferase can exist as a catalytically active NADase.

6 In agreement, NADase activity in the plasma of eviscerated DR-BB rats

7 -ribose; and (iv) purified HvnA displayed an NADase V(max) of 400 mol min(-1) mol(-1), which is withi

8 two modifications and converted ART5 from an NADase to a transferase, and could be one mechanism for

9 ART5 was found to be primarily an NADase at 10 microM NAD, whereas at higher NAD concentra

10 cine can turn ADPRC from a cyclase toward an NADase.

11 A double mutant lacking SLO and NADase activity had an intermediate virulence phenotype,

12 ignificantly increased production of SLO and NADase.

13 e mechanism of regulation of transferase and NADase activities, ART5 was synthesized as a FLAG fusion

14 Furthermore, because NADase-negative strains did not produce immunoreactive N

15 Production of both NADase and SLO is associated with augmented host cell in

16 Purified recombinant SLO bound NADase in vitro, supporting a specific, physical interac

17 augmentation of SLO-mediated cytotoxicity by NADase is a consequence of depletion of host cell energy

18 a GPI anchor; ART2- T cell subsets contained NADase activity that was not releasable by phosphatidyli

19 hat additional regulatory element(s) control NADase production.

20 orms pores in the cell membrane and delivers NADase to the epithelial cell cytoplasm.

21 auto-ADP-ribosylated and exhibited enhanced NADase activity.

22 been deleted (GST-Yac-1-delta121), exhibited NADase, but not transferase, activity.

23 lly all M-1 GAS were previously negative for NADase.

24 trains isolated after 1988 were positive for NADase, whereas virtually all M-1 GAS were previously ne

25 ype parent, confirming an important role for NADase in the infection of a host animal.

26 z)AD(+) and N(tz)ADH serve as substrates for NADase, which selectively cleaves the nicotinamide's gly

27 Furthermore, NADase activity did not correlate with invasive disease

28 Furthermore, expression of recombinant GAS NADase in yeast, in the absence of SLO, induced growth a

29 presence of cell surface NAD glycohydrolase (NADase) activities.

30 I)-anchored, whereas the NAD glycohydrolase (NADase) activity remained cell-associated.

31 it exhibited significant NAD glycohydrolase (NADase) activity.

32 e) and the production of NAD glycohydrolase (NADase).

33 on and diverging into NAD(+) glycohydrolase (NADase)-active and -inactive subtypes.

34 indirectly through an NAD(+)-glycohydrolase (NADase) activity that releases free, reactive, ADP-ribos

35 eptolysin O (SLO) and NAD(+)-glycohydrolase (NADase), have been shown to interact functionally as a c

36 e adenine dinucleotide (NAD) glycohydrolase (NADase) and auto-ADP-ribosyltransferase activities.

37 he extracellular toxins NAD+-glycohydrolase (NADase) and streptolysin O (SLO).

38 the translocation of GAS NAD-glycohydrolase (NADase) into human epithelial cells in vitro.

39 ) and ART2b (RT6.2) are NAD glycohydrolases (NADases) that are linked to T lymphocytes by glycosylpho

40 and degradation, as well as NAD hydrolysis (NADase).

41 ative strains did not produce immunoreactive NADase, we concluded that additional regulatory element(

42 erase bands of 38 kDa and the immunoreactive NADase band of approximately 18 kDa.

43 All mutants were immunoreactive NADases.

44 and E146L showed 7- and 19-fold reduction in NADase activity, respectively.

45 izing folding of the substrate, resulting in NADase being the dominant activity.

46 ber of a widespread family of interbacterial NADases predicted to transit not only the Gram-negative

47 at the SARM1-TIR domain itself has intrinsic NADase activity-cleaving NAD(+) into ADP-ribose (ADPR),

48 In both models, mutant GAS that lacked NADase activity were significantly attenuated for virule

49 d 10(2)- to 10(4)-fold higher than the minor NADase activity reported in bacterial ARTase toxins.

50 nergy stores through the enzymatic action of NADase.

51 ation by cADPR hydrolase and the activity of NADase was increased, but to a much lesser degree than a

52 strain, which correlated with the amount of NADase and SLO activities in culture supernatant fluids.

53 ic GAS mutants to assess the contribution of NADase activity to GAS virulence in vivo using mouse mod

54 evealed a previously unknown contribution of NADase to the cytolytic activity associated with GAS pro

55 We have now shown that expression of NADase together with SLO dramatically enhanced the lytic

56 ion of apoptosis; however, the importance of NADase during infection of an animal host has not been e

57 In summary, the temporal relationship of NADase expression, alone or with other streptococcal vir

58 ADase activity, consistent with at least one NADase having a GPI anchor; ART2- T cell subsets contain

59 sis of an hvnA hvnB mutant revealed no other NADase activity in culture supernatants of V. fischeri,

60 which is within the range reported for other NADases and 10(2)- to 10(4)-fold higher than the minor N

61 s free, reactive, ADP-ribose: (i) like other NADases, and in contrast to the ARTase cholera toxin, Hv

62 BB rats with anti-RT6.1 mAb increased plasma NADase activity, which localized, by fluid phase liquid

63 ounts of the secreted cytotoxins S. pyogenes NADase (SPN) and streptolysin O (SLO).

64 ces the chromosomal region encoding secreted NADase and streptolysin O, is the key driver of increase

65 his effector, termed Tne2 (Type VI secretion NADase effector family 2), demonstrates that it possesse

66 40 kDa and that of the detergent-solubilized NADase was approximately 100 kDa.

67 We conclude that NADase and SLO together enhance GAS virulence in vivo.

68 Additionally, the NADase-inactive SPN subtypes maintain the characteristic

69 lization (cyclase) reaction of ADPRC and the NADase reaction of CD38.

70 NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W),

71 band were visualized among proteins from the NADase fractions and 38-40-kDa bands with protein from t

72 specific phospholipase C removed much of the NADase activity, consistent with at least one NADase hav

73 y models in neurons, we demonstrate that the NADase activity of full-length SARM1 is required in axon

74 A good correlation was observed when the NADase activity of all the mutants was plotted against t

75 zed in a two-step process, starting with the NADase-catalyzed exchange of a synthetic nicotinamide de

76 Thus, NADase-inactive SPN continues to evolve under functional

77 lay, transferase activity increased, whereas NADase activity fell.

78 in ("specialist" strains) is associated with NADase-inactive SPN.

79 in ("generalist" strains) is correlated with NADase-active SPN, while the preference for causing infe

80 In vitro, intoxication of keratinocytes with NADase is associated with cytotoxic effects and inductio