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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 specific, nicotinamide adenine dinucleotide (NAD(+)) depletion.
8 ulation of Mcl-1; (2) enhanced intracellular NAD(+) depletion; (3) inhibition of chymotrypsin-like, c
10 leted cells undergo PARP hyperactivation and NAD depletion after severe DNA damage but, unlike wild-t
11 ate, points to reduced oxidative flux due to NAD(+) depletion after beta-lapachone treatment of NQO1+
12 sphate (cGMP) in response to dietary sodium (Na) depletion alone, or Na depletion or normal Na diet c
14 nce of glucose (Glu(-) cells) is followed by NAD depletion and an unexpected PARP-1 activity-dependen
16 SARM1 is required in axons to promote axonal NAD(+) depletion and axonal degeneration after injury.
17 ly(ADP-ribose) polymerase 1 (PARP1) leads to NAD(+) depletion and cell death during ischemia and othe
18 vent in PARP-1-mediated cell death and place NAD(+) depletion and glycolytic failure upstream of mito
23 sponse to nicotinamide adenine dinucleotide (NAD) depletion and in diabetic mouse and human livers.
24 ARP-1 was confirmed by direct measurement of NAD+ depletion and ADP-ribose polymer formation caused b
26 e potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtui
31 lar NAD, activation of ADPRT, and subsequent NAD depletion during apoptosis in KG1a, YAC-1, and BW154
35 inhibition of hexokinase, which precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine
37 vation of the reninangiotensin system during Na depletion increases renal interstitial PGE2 and cGMP.
40 ells treated with doxorubicin, which induces NAD depletion, led to a rebound in intracellular levels
42 rotects neurons against homocysteine-induced NAD depletion, loss of mitochondrial transmembrane poten
43 ic signaling, and suggest that prevention of NAD depletion may be critical in the treatment of cardia
44 The resulting cell death was preceded by NAD(+) depletion, mitochondrial membrane depolarization,
45 ion of poly-ADP-ribose polymerase (PARP) and NAD depletion occur rapidly after exposure to homocystei
46 e to dietary sodium (Na) depletion alone, or Na depletion or normal Na diet combined with the AT1 rec
51 mediated hypoxic signaling pathway involving NAD(+) depletion, SIRT1 inhibition, FoxO3a-driven Bnip3
52 herapeutic approaches inducing intracellular NAD(+) depletion, such as alkylating agents or direct NA
53 ARG inhibitor gallotannin both prevented the NAD(+) depletion that otherwise results from PARP1 activ
54 Na+-depleted diet; however, after 2 weeks of Na+ depletion the mean arterial blood pressure of Ncc-/-
56 oribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribos
60 al and sham drinking of NaCl solutions after Na depletion with the diuretic furosemide (10 mg/kg).
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