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1  was markedly and specifically reduced after NA depletion.
2 liking in rats with and without a history of Na+ depletion.
3 the pathways leading to cell death following NAD depletion.
4 hat ATP loss is not metabolically related to NAD depletion.
5 ibose polymerase and prevention of beta-cell NAD depletion.
6 lowing PARP-1 activation is not dependent on NAD(+) depletion.
7 1 activity in the SCA7 mouse cerebellum with NAD(+) depletion.
8 sis in a mouse model of SSc characterized by NAD(+) depletion.
9 specific, nicotinamide adenine dinucleotide (NAD(+)) depletion.
10 -mediated nicotinamide adenine dinucleotide (NAD(+)) depletion.
11 ulation of Mcl-1; (2) enhanced intracellular NAD(+) depletion; (3) inhibition of chymotrypsin-like, c
12                                              NAD+ depletion activated the intracellular energy sensor
13 leted cells undergo PARP hyperactivation and NAD depletion after severe DNA damage but, unlike wild-t
14 ate, points to reduced oxidative flux due to NAD(+) depletion after beta-lapachone treatment of NQO1+
15 sphate (cGMP) in response to dietary sodium (Na) depletion alone, or Na depletion or normal Na diet c
16                            Prolonged dietary Na+ depletion and chronic administration of adrenal ster
17 nce of glucose (Glu(-) cells) is followed by NAD depletion and an unexpected PARP-1 activity-dependen
18 y(ADP-ribose) polymerase-1 (PARP-1) triggers NAD depletion and cell death.
19                                              NAD(+) depletion and autophagy induced by NAMPT inhibito
20 SARM1 is required in axons to promote axonal NAD(+) depletion and axonal degeneration after injury.
21 ly(ADP-ribose) polymerase 1 (PARP1) leads to NAD(+) depletion and cell death during ischemia and othe
22 ag(-/-) cells are protected from MMS-induced NAD(+) depletion and glycolysis inhibition.
23 vent in PARP-1-mediated cell death and place NAD(+) depletion and glycolytic failure upstream of mito
24                            Here we show that NAD(+) depletion and mitochondrial permeability transiti
25         PARP-1 activation leads to cytosolic NAD(+) depletion and mitochondrial release of apoptosis-
26                   These results suggest that NAD(+) depletion and MPT are necessary intermediary step
27                                     Neuronal NAD(+) depletion and poly(ADP-ribose) formation, which a
28 sponse to nicotinamide adenine dinucleotide (NAD) depletion and in diabetic mouse and human livers.
29 ARP-1 was confirmed by direct measurement of NAD+ depletion and ADP-ribose polymer formation caused b
30                                          The NAD+ depletion and inhibition of mitochondrial respirati
31 e potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtui
32                      These results establish NAD(+) depletion as a causal event in PARP-1-mediated ce
33                                  We identify NAD(+) depletion as central to the glycolytic inhibition
34                            Thus, we identify NAD+ depletion as a metabolic susceptibility of IDH1 mut
35  one theory postulates an essential role for NAD depletion by poly-ADP-ribose polymerase.
36                                  Strikingly, NAD(+) depletion by light activation of Ru-STF31 in hypo
37                              The accelerated NAD depletion did not seem to interfere with the later s
38 lar NAD, activation of ADPRT, and subsequent NAD depletion during apoptosis in KG1a, YAC-1, and BW154
39  are associated with cellular senescence and NAD + depletion in dogs and people.
40 ing a requirement for PARP activation and/or NAD depletion in homocysteine-induced apoptosis.
41 t-induced apoptotic cell death is not due to NAD depletion in some leukemia cell lines.
42  gene that is activated by energy stress and NAD(+) depletion in isolated rat cardiomyocytes.
43 inhibition of hexokinase, which precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine
44                                 In contrast, NA depletion increased the expression of the sleep-relat
45 vation of the reninangiotensin system during Na depletion increases renal interstitial PGE2 and cGMP.
46                                         This Na(+) depletion is accompanied by K(+) accumulation and
47                                              NAD(+) depletion is a common phenomenon in neurodegenera
48                         To determine whether NAD(+) depletion is necessary for PARP-1-induced MPT, NA
49 ells treated with doxorubicin, which induces NAD depletion, led to a rebound in intracellular levels
50                                       During Na depletion, Losartan decreased PGE2 and did not change
51 rotects neurons against homocysteine-induced NAD depletion, loss of mitochondrial transmembrane poten
52 ic signaling, and suggest that prevention of NAD depletion may be critical in the treatment of cardia
53     The resulting cell death was preceded by NAD(+) depletion, mitochondrial membrane depolarization,
54 ion of poly-ADP-ribose polymerase (PARP) and NAD depletion occur rapidly after exposure to homocystei
55 ubstantially protected from high fat-induced NAD(+) depletion, oligodendrocyte loss, oxidative damage
56             However, the potential impact of NAD(+) depletion on the brain tumor microenvironment has
57 e to dietary sodium (Na) depletion alone, or Na depletion or normal Na diet combined with the AT1 rec
58      Remarkably, mitochondrial uncouplers or Na+ depletion prevent the ability of T cells to maintain
59                                We found that NA depletion reduces the expression of approximately 20%
60                  Toxic prion protein-induced NAD(+) depletion results from PARP1-independent excessiv
61                                              Na depletion significantly increased PGE2 and cGMP.
62 mediated hypoxic signaling pathway involving NAD(+) depletion, SIRT1 inhibition, FoxO3a-driven Bnip3
63 gnal pathway was inhibited by FK866-mediated NAD(+) depletion, specifically TAK1, IKKbeta, IkBalpha,
64 demonstrate that macroH2A1 prevents cellular NAD(+) depletion, subsequently preventing necrotic cell
65 herapeutic approaches inducing intracellular NAD(+) depletion, such as alkylating agents or direct NA
66 ARG inhibitor gallotannin both prevented the NAD(+) depletion that otherwise results from PARP1 activ
67 Na+-depleted diet; however, after 2 weeks of Na+ depletion the mean arterial blood pressure of Ncc-/-
68 sveratrol, curcumin) and agents that prevent NAD depletion (theophylline) upregulate SIRT1 and reduce
69                              Concurrent with NAD depletion, there was a decrease in both cell prolife
70                                              NAD(+) depletion triggers axonal degeneration, which is
71 oribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribos
72                                      Dietary Na(+) depletion was used to induce secondary hyperaldost
73                        However, a history of Na+ depletion was not associated with a greater positive
74 cts of this drug on energy metabolism due to NAD(+) depletion were never described.
75                    Conversely, intracellular Na+ depletion, which inhibits Na+-dependent Ca2+ export
76 al and sham drinking of NaCl solutions after Na depletion with the diuretic furosemide (10 mg/kg).
77 s in LPS-exposed monocytes were inhibited by NAD(+) depletion with FK866, 3) the inhibition was not c