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1                                              NMN appeared to have stronger effects on liver fat catab
2                                              NMN deamidase, a bacterial enzyme, shares NMN-consuming
3                                              NMN is a rate-limiting precursor for recycling to the es
4                                              NMN is a substrate of both ectoenzymes CD38 and CD73, wi
5                                              NMN synthesis by NAMPT is powerfully inhibited by both N
6 rt a pro-degenerative effect of accumulating NMN in axons in vivo.
7 ntral domain has a weak adenylyltransferase (NMN-AT; EC 2.7.7.1) activity that converts NMN directly
8 deficits, we compared treadmill exercise and NMN injection in offspring of obese mothers.
9 ate-limiting for the use of exogenous NR and NMN for NAD(+) synthesis.
10     Inhibition is observed with reduced beta-NMN and alpha-NADH, but neither is as effective as beta-
11  select for increased discrimination between NMN and NMNH.
12  to be a bifunctional enzyme possessing both NMN adenylytransferase (NMNAT; EC ) and ribosylnicotinam
13 strate specificity of the enzyme toward both NMN and NaMN and reveal the structural mechanism for ade
14 nique dual substrate specificity toward both NMN and NaMN, thus flexible in participating in both de
15               The first step is catalyzed by NMN synthetase, which was identified and characterized i
16 red NAD(+) and MgCl(2), and was inhibited by NMN and AMP, products of the ligase reaction.
17              The second step is performed by NMN adenylyltransferase of the NadM family.
18 lters an ATP-binding residue in the central (NMN-AT) domain.
19 table isotope-labelled compounds, we confirm NMN is metabolized extracellularly to NR that is then ta
20  (NMN-AT; EC 2.7.7.1) activity that converts NMN directly to NAD but is physiologically irrelevant.
21 (NMN) in zebrafish and mice, which decreases NMN levels by converting it to NaMN, protects against ax
22                              This eliminates NMN-AT activity and places the enzyme in its default (DN
23     Unlike other yeast NMNATs, Pof1 exhibits NMN-specific adenylyltransferase activity.
24 D38 impairs, the conversion of extracellular NMN to NR as a precursor for intracellular NAD(+) biosyn
25 an cells require conversion of extracellular NMN to NR for cellular uptake and NAD(+) synthesis, expl
26 reated cells supplemented with extracellular NMN was strongly reduced in tumor cells, upon pharmacolo
27                                 The kcat for NMN+ was 5-fold higher than that of NAD+ and has the gre
28 N aptamer sequences was used to reselect for NMN binding.
29 as identified that increases specificity for NMN.
30 (Nmnat2) catalyzes the synthesis of NAD from NMN and ATP.
31     In route 1, nicotinamide is removed from NMN in the periplasm and enters the cell as the free bas
32 2, described here, phosphate is removed from NMN in the periplasm by acid phosphatase (AphA), and the
33  validation of the predicted route (NaMN --> NMN --> NAD) in F. tularensis including mathematical mod
34 y in pnuC* transporter mutants, which import NMN intact and can therefore grow on lower levels of NMN
35                                     Internal NMN produced by either route 2 or route 3 is deamidated
36                   In contrast to other known NMN ATs, biophysical characterizations reveal it to be a
37 ammonium (TBuMA), and N'-methylnicotinamide (NMN).
38 cting stem-loops is proposed for the minimal NMN-binding RNA.
39 cterial nicotinamide adenine mononucleotide (NMN) in zebrafish and mice, which decreases NMN levels b
40                 Nicotinamide mononucleotide (NMN) adenylyltransferase 2 (Nmnat2) catalyzes the synthe
41 le synthesis of nicotinamide mononucleotide (NMN) and inorganic pyrophosphate (PP i) from nicotinamid
42 ccumulations of nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) in the amidated salv
43 (+) precursors, nicotinamide mononucleotide (NMN) and NR, can reverse the FK866-induced cell death, t
44 th NaMN and the nicotinamide mononucleotide (NMN) but shows specificity for the nicotinate.
45  from exogenous nicotinamide mononucleotide (NMN) by three routes.
46 D(+) precursor, nicotinamide mononucleotide (NMN) can reverse some of the negative consequences of hi
47 N) and mediates nicotinamide mononucleotide (NMN) catabolism, thereby contributing to both NmR salvag
48 osphorolysis of nicotinamide mononucleotide (NMN) from kinetic isotope effects (KIEs).
49 n (Rb) and beta-nicotinamide mononucleotide (NMN) have been isolated by in vitro selection.
50 AD(+) precursor nicotinamide mononucleotide (NMN) increases BubR1 abundance in vivo.
51 cleoside of the nicotinamide mononucleotide (NMN) leaving group are oriented solely via atomic intera
52 tion of NaMN to nicotinamide mononucleotide (NMN) occurs before the adenylylation reaction, which con
53 ursors, such as nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR), protects against met
54 zymatic product nicotinamide mononucleotide (NMN), was not blocked by the Nampt enzyme inhibitor FK86
55  an alternative nicotinamide mononucleotide (NMN)-preferring adenylyltransferase (slr0787 gene).
56 t internally to nicotinamide mononucleotide (NMN).
57      Nicotinamide/nicotinate mononucleotide (NMN/ NaMN)adenylyltransferase (NMNAT) is an indispensabl
58 the condensation of pyridine mononucleotide (NMN or NaMN) with the AMP moiety of ATP to form NAD (or
59 by the organic cation n-methyl-nicotinamide (NMN), being instead stimulated by it (fourfold).
60 non-deamidating utilization of nicotinamide (NMN shunt).
61                   Like overexpressed NMNATs, NMN deamidase reduces NMN accumulation in injured mouse
62 was downregulated and so the accumulation of NMN and NR was best explained by reduced flux through th
63 ct and can therefore grow on lower levels of NMN.
64 ve ATPase activity, allows the production of NMN at product:substrate ratios thermodynamically forbid
65  further study to confirm the suitability of NMN for use in reversing metabolic dysfunction linked to
66 strates and NAD(+), and the IC(50) values of NMN and AMP, examined the effects of MgCl(2) and PEG(800
67 ere given treadmill exercise for 9 weeks, or NMN injection daily for 18 days.
68 rom their precursors, 4'-phosphopantetheine, NMN, and FMN, respectively.
69  overexpressed NMNATs, NMN deamidase reduces NMN accumulation in injured mouse sciatic nerves and pre
70                                  Remarkably, NMN deamidase also rescues axonal outgrowth and perinata
71    NMN deamidase, a bacterial enzyme, shares NMN-consuming activity with NMNAT2, but not NAD-synthesi
72 l by maintaining low levels of its substrate NMN rather than generating NAD; however, this is still d
73                     Noncyclizable substrates NMN+ and nicotinamide-7-deaza-hypoxanthine dinucleotide
74  complex of CD38 with one of its substrates, NMN, showed that the nicotinamide moiety was in close co
75                 With the natural substrates, NMN and pyrophosphate (PPi), the intrinsic KIEs of [1'-(
76                            Here we show that NMN deamidase can also delay axon degeneration in zebraf
77                                          The NMN deamidase mouse will be an important tool to further
78 14); (ii) comprise the interface between the NMN-binding domain (domain Ia) and the nucleotidyltransf
79       A mutagenized pool based on one of the NMN aptamer sequences was used to reselect for NMN bindi
80   Together with the crystal structure of the NMN.PPi.Mg2.enzyme complex, the reaction coordinate is d
81 itors with oxacarbenium mimics replacing the NMN-ribosyl group of NAD(+) show 200-620-fold increased
82       Internal NmR is then converted back to NMN by the NmR kinase activity of NadR.
83               With ATP hydrolysis coupled to NMN synthesis, the catalytic efficiency of the system is
84 M), and the K eq shifts -2.1 kcal/mol toward NMN formation.
85 e catalytic domain is flanked by an upstream NMN-binding module and by downstream OB-fold, zinc finge
86                       To investigate whether NMN can impact developmentally-set metabolic deficits, w

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