ライフサイエンスコーパス: Na depletion

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

9 NAD+ depletion activated the intracellular energy sensor

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

13 Prolonged dietary Na+ depletion and chronic administration of adrenal ster

14 nce of glucose (Glu(-) cells) is followed by NAD depletion and an unexpected PARP-1 activity-dependen

15 y(ADP-ribose) polymerase-1 (PARP-1) triggers NAD depletion and cell death.

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

19 Here we show that NAD(+) depletion and mitochondrial permeability transiti

20 PARP-1 activation leads to cytosolic NAD(+) depletion and mitochondrial release of apoptosis-

21 These results suggest that NAD(+) depletion and MPT are necessary intermediary step

22 Neuronal NAD(+) depletion and poly(ADP-ribose) formation, which a

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

25 The NAD+ depletion and inhibition of mitochondrial respirati

26 e potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtui

27 These results establish NAD(+) depletion as a causal event in PARP-1-mediated ce

28 Thus, we identify NAD+ depletion as a metabolic susceptibility of IDH1 mut

29 one theory postulates an essential role for NAD depletion by poly-ADP-ribose polymerase.

30 The accelerated NAD depletion did not seem to interfere with the later s

31 lar NAD, activation of ADPRT, and subsequent NAD depletion during apoptosis in KG1a, YAC-1, and BW154

32 ing a requirement for PARP activation and/or NAD depletion in homocysteine-induced apoptosis.

33 t-induced apoptotic cell death is not due to NAD depletion in some leukemia cell lines.

34 gene that is activated by energy stress and NAD(+) depletion in isolated rat cardiomyocytes.

35 inhibition of hexokinase, which precedes the NAD(+) depletion in N-methyl-N-nitroso-N-nitroguanidine

36 In contrast, NA depletion increased the expression of the sleep-relat

37 vation of the reninangiotensin system during Na depletion increases renal interstitial PGE2 and cGMP.

38 NAD(+) depletion is a common phenomenon in neurodegenera

39 To determine whether NAD(+) depletion is necessary for PARP-1-induced MPT, NA

40 ells treated with doxorubicin, which induces NAD depletion, led to a rebound in intracellular levels

41 During Na depletion, Losartan decreased PGE2 and did not change

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

47 Remarkably, mitochondrial uncouplers or Na+ depletion prevent the ability of T cells to maintain

48 We found that NA depletion reduces the expression of approximately 20%

49 Toxic prion protein-induced NAD(+) depletion results from PARP1-independent excessiv

50 Na depletion significantly increased PGE2 and cGMP.

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-/-

55 Concurrent with NAD depletion, there was a decrease in both cell prolife

56 oribosyltransferase (Naprt1), sensitizing to NAD+ depletion via concomitant nicotinamide phosphoribos

57 However, a history of Na+ depletion was not associated with a greater positive

58 cts of this drug on energy metabolism due to NAD(+) depletion were never described.

59 Conversely, intracellular Na+ depletion, which inhibits Na+-dependent Ca2+ export

60 al and sham drinking of NaCl solutions after Na depletion with the diuretic furosemide (10 mg/kg).