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1                                              NADase (SPN) and streptolysin O (SLO) are two toxins tha
2                                              NADase purified from GAS altered neutrophil-directed mig
3 1 (sterile alpha and TIR motif containing 1) NADase.
4        These findings suggest that SPN has a NADase-independent function and prompt a reevaluation of
5 keratinocytes to wild-type GAS, but not to a NADase-deficient mutant strain, resulted in profound dep
6 process driven by SARM1, an injury-activated NADase.
7 nsferase can exist as a catalytically active NADase.
8 heral ring, which allows formation of active NADase domain dimers, thereby further depleting NAD+ to
9                                In agreement, NADase activity in the plasma of eviscerated DR-BB rats
10 -ribose; and (iv) purified HvnA displayed an NADase V(max) of 400 mol min(-1) mol(-1), which is withi
11 two modifications and converted ART5 from an NADase to a transferase, and could be one mechanism for
12               We demonstrate that SpbK is an NADase that produces both ADP-ribose (ADPR) and canonica
13 ependent TIR function using nicotinamide, an NADase inhibitor.
14            ART5 was found to be primarily an NADase at 10 microM NAD, whereas at higher NAD concentra
15 cine can turn ADPRC from a cyclase toward an NADase.
16              A double mutant lacking SLO and NADase activity had an intermediate virulence phenotype,
17 ignificantly increased production of SLO and NADase.
18 e mechanism of regulation of transferase and NADase activities, ART5 was synthesized as a FLAG fusion
19 se from each other and other T6SS-associated NADases.
20 y between human STING genotype and bacterial NADase activity.
21  an immune-regulating function for bacterial NADase and provide insight regarding the host-pathogen g
22 inding capacity combined with high bacterial NADase activity promotes a 'perfect storm' manifested in
23                         Furthermore, because NADase-negative strains did not produce immunoreactive N
24 ies of SpbK TIR domains is required for both NADase activity and antiphage defence.
25                           Production of both NADase and SLO is associated with augmented host cell in
26               Purified recombinant SLO bound NADase in vitro, supporting a specific, physical interac
27 augmentation of SLO-mediated cytotoxicity by NADase is a consequence of depletion of host cell energy
28 eractivation of stress responses mediated by NADases of PARP and Sirtuin families.
29 e NAD metabolome that includes elevated CD38 NADase and reduced poly(ADP-ribose) polymerase and SIRT1
30                             The constitutive NADase activity of these seven variants is similar to th
31 a GPI anchor; ART2- T cell subsets contained NADase activity that was not releasable by phosphatidyli
32 hat additional regulatory element(s) control NADase production.
33               SARM1, a protein with critical NADase activity, is a central executioner in a conserved
34 orms pores in the cell membrane and delivers NADase to the epithelial cell cytoplasm.
35  defend against phage infection by deploying NADase effectors to degrade cellular NAD(+), thereby hal
36 an executor of axonal degeneration, displays NADase activity that depletes the key cellular metabolit
37 facilitated the inhibition of the TIR-domain NADase through the domain interface.
38  auto-ADP-ribosylated and exhibited enhanced NADase activity.
39  both bacterial TIR NAD(+)-cleaving enzymes (NADases) and the mammalian SARM1 (sterile alpha and TIR
40 te for a series of NAD(+)-consuming enzymes (NADases), including PARPs and SIRTs.
41 been deleted (GST-Yac-1-delta121), exhibited NADase, but not transferase, activity.
42 quirement of TIR domain self-association for NADase activity and axon degeneration.
43 lly all M-1 GAS were previously negative for NADase.
44 trains isolated after 1988 were positive for NADase, whereas virtually all M-1 GAS were previously ne
45  identifies conserved functions required for NADase activity and reveals that unrelated NADase immuni
46 ype parent, confirming an important role for NADase in the infection of a host animal.
47 z)AD(+) and N(tz)ADH serve as substrates for NADase, which selectively cleaves the nicotinamide's gly
48                       We propose that fungal NADases may convey advantages during interaction with th
49                                 Furthermore, NADase activity did not correlate with invasive disease
50   Furthermore, expression of recombinant GAS NADase in yeast, in the absence of SLO, induced growth a
51 presence of cell surface NAD glycohydrolase (NADase) activities.
52 I)-anchored, whereas the NAD glycohydrolase (NADase) activity remained cell-associated.
53 it exhibited significant NAD glycohydrolase (NADase) activity.
54 e) and the production of NAD glycohydrolase (NADase).
55 on and diverging into NAD(+) glycohydrolase (NADase)-active and -inactive subtypes.
56 indirectly through an NAD(+)-glycohydrolase (NADase) activity that releases free, reactive, ADP-ribos
57 eptolysin O (SLO) and NAD(+)-glycohydrolase (NADase), have been shown to interact functionally as a c
58 e adenine dinucleotide (NAD) glycohydrolase (NADase) and auto-ADP-ribosyltransferase activities.
59 he extracellular toxins NAD+-glycohydrolase (NADase) and streptolysin O (SLO).
60 the translocation of GAS NAD-glycohydrolase (NADase) into human epithelial cells in vitro.
61 ) and ART2b (RT6.2) are NAD glycohydrolases (NADases) that are linked to T lymphocytes by glycosylpho
62 f life act in defense responses and can have NADase activity that hydrolyzes NAD(+).
63   TIR domains across different kingdoms have NADase activities and can produce phosphoribosyl adenosi
64 nicotinamide adenine dinucleotide hydrolase (NADase) sterile alpha toll/interleukin receptor motif co
65 hich engaged its intrinsic NAD(+) hydrolase (NADase) activity to activate the p38 innate immune pathw
66 TIR) proteins function as NAD(+) hydrolases (NADase) links NAD(+)-derived small molecules with immune
67  and degradation, as well as NAD hydrolysis (NADase).
68 ative strains did not produce immunoreactive NADase, we concluded that additional regulatory element(
69 erase bands of 38 kDa and the immunoreactive NADase band of approximately 18 kDa.
70              All mutants were immunoreactive NADases.
71 and E146L showed 7- and 19-fold reduction in NADase activity, respectively.
72 izing folding of the substrate, resulting in NADase being the dominant activity.
73 ells; they lack constitutive and NMN-induced NADase activity; and they fail to promote axon degenerat
74 R motif containing 1 (SARM1) is an inducible NADase that localizes to mitochondria throughout neurons
75                                   Inhibiting NADase activity of CD38 reinvigorated the metabolism and
76 ber of a widespread family of interbacterial NADases predicted to transit not only the Gram-negative
77                  SARM1 contains an intrinsic NADase enzymatic activity essential for its pro-degenera
78 at the SARM1-TIR domain itself has intrinsic NADase activity-cleaving NAD(+) into ADP-ribose (ADPR),
79 o contribute to axon degeneration due to its NADase activity.
80 chanism that is distinct from those of known NADases, ADP-ribosyl cyclases and transferases.
81       In both models, mutant GAS that lacked NADase activity were significantly attenuated for virule
82               We identified CD38 as the main NADase up-regulated in reactive mouse and human astrocyt
83 d 10(2)- to 10(4)-fold higher than the minor NADase activity reported in bacterial ARTase toxins.
84  10), whereas those of pro-neurodegenerative NADase Sterile Alpha and TIR motif-containing protein 1
85 otinamide adenine dinucleotide nucleotidase (NADase) CD38.
86 nergy stores through the enzymatic action of NADase.
87 ation by cADPR hydrolase and the activity of NADase was increased, but to a much lesser degree than a
88 ain competition and the repeated adoption of NADase toxins as weapons against bacterial cells.
89  strain, which correlated with the amount of NADase and SLO activities in culture supernatant fluids.
90 ic GAS mutants to assess the contribution of NADase activity to GAS virulence in vivo using mouse mod
91 evealed a previously unknown contribution of NADase to the cytolytic activity associated with GAS pro
92         We have now shown that expression of NADase together with SLO dramatically enhanced the lytic
93 ion of apoptosis; however, the importance of NADase during infection of an animal host has not been e
94     In summary, the temporal relationship of NADase expression, alone or with other streptococcal vir
95 ctivity but belong to different subgroups of NADase from each other and other T6SS-associated NADases
96        Here, we report the identification of NADases on the surface of fungi such as the pathogen Asp
97 ADase activity, consistent with at least one NADase having a GPI anchor; ART2- T cell subsets contain
98 sis of an hvnA hvnB mutant revealed no other NADase activity in culture supernatants of V. fischeri,
99 which is within the range reported for other NADases and 10(2)- to 10(4)-fold higher than the minor N
100 s free, reactive, ADP-ribose: (i) like other NADases, and in contrast to the ARTase cholera toxin, Hv
101 BB rats with anti-RT6.1 mAb increased plasma NADase activity, which localized, by fluid phase liquid
102 for type III effectors (T3Es) with potential NADase activity.
103 ounts of the secreted cytotoxins S. pyogenes NADase (SPN) and streptolysin O (SLO).
104          Various bacterial pathogens release NADase enzymes into the host cell that deplete the host'
105        Thus, plant TIR-NLR receptors require NADase function to transduce recognition of pathogens in
106                                        SARM1 NADase activity is activated by the NAD(+) precursor nic
107 l factors NMNAT2 and STMN2 to activate SARM1 NADase activity, which leads to calcium influx and axon
108          Using a biochemical assay for SARM1 NADase we identified a novel series of potent and select
109 omain and constitutively hyperactivate SARM1 NADase activity.
110 iating high-affinity inhibition of the SARM1 NADase.
111   Our studies support a model in which SARM1 NADase activity leads to an ordered sequence of events f
112 ces the chromosomal region encoding secreted NADase and streptolysin O, is the key driver of increase
113 his effector, termed Tne2 (Type VI secretion NADase effector family 2), demonstrates that it possesse
114 es protection against T6SS-delivered SJC1036 NADase.
115 40 kDa and that of the detergent-solubilized NADase was approximately 100 kDa.
116                             We conclude that NADase and SLO together enhance GAS virulence in vivo.
117      Mechanistically, it has been shown that NADases can directly regulate autophagy and mitochondria
118                                          The NADase SARM1 (sterile alpha and TIR motif containing 1)
119 odecameric portal protein that activates the NADase function of SpbK by facilitating TIR domain clust
120                            Additionally, the NADase-inactive SPN subtypes maintain the characteristic
121 lization (cyclase) reaction of ADPRC and the NADase reaction of CD38.
122 on degeneration, nor is it determined by the NADase activity of TIR-1.
123  NAD and auto-ADP-ribosylation decreased the NADase activities of wild-type ART2b and ART2b (R204W),
124 on, and a C-terminal TIR domain encoding the NADase enzyme.
125 band were visualized among proteins from the NADase fractions and 38-40-kDa bands with protein from t
126         These covalent compounds inhibit the NADase activity of WT-SARM1, but not C311A or C311S SARM
127 specific phospholipase C removed much of the NADase activity, consistent with at least one NADase hav
128       However, the enzymatic activity of the NADase variants expressed by invasive strains suppresses
129 y models in neurons, we demonstrate that the NADase activity of full-length SARM1 is required in axon
130     A good correlation was observed when the NADase activity of all the mutants was plotted against t
131 zed in a two-step process, starting with the NADase-catalyzed exchange of a synthetic nicotinamide de
132 rts its pro-neurodegenerative action through NADase activity(9,10).
133                                        Thus, NADase-inactive SPN continues to evolve under functional
134                                 SARM1, a TIR NADase with a pivotal role in axonal degeneration, coloc
135 and coordinate packing of the associated TIR NADase effector domains at the base of the filament to d
136 sults provide insight into how bacterial TIR NADases recognise phage infection.
137 r NADase activity and reveals that unrelated NADase immunity proteins utilise a common mechanism of e
138 lay, transferase activity increased, whereas NADase activity fell.
139 in ("specialist" strains) is associated with NADase-inactive SPN.
140 in ("generalist" strains) is correlated with NADase-active SPN, while the preference for causing infe
141 In vitro, intoxication of keratinocytes with NADase is associated with cytotoxic effects and inductio
142 d from catabolism of NAD(+) by proteins with NADase activity (e.g., PARPs, SIRTs, CD38).

 
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