ライフサイエンスコーパス: NLA

1 NLA blocked NO increase in endothelial cells under hyper

2 NLA infusion decreased RIHP to 1.9+/-0.5 mm Hg and also

3 NLA treatment decreased RBF (5.3+/-0.3 to 3.6+/-0.2 ml/m

4 R827 and its NITROGEN LIMITATION ADAPTATION (NLA) target gene in mediating plant susceptibility to th

5 n E3 ligase, nitrogen limitation adaptation (NLA).

6 The NITROGEN LIMITATION ADAPTION (NLA) gene was initially shown to function in nitrogen li

7 After NLA, there was no measurable NO production at rest or du

8 The metabolic changes after NLA occurred in the absence of alterations in myocardial

9 is was known as the Northern Liver Alliance (NLA) "top-band scheme." Organs were shared between the 3

10 al microscopy of fusion proteins revealed an NLA/PT2 interaction at the plasma membrane.

11 s nerve caused greater increases in CBF, and NLA inhibited increases in CBF.

12 ACh levels (pmol/10 min) during control and NLA dialysis, respectively, were 0.58 +/- 0.03 and 0.77

13 bolites and miRNA comparing CTL with NLA and NLA with PLS, identified several hubs of metabolite and

14 c oxide synthase inhibitor nitro-L-arginine (NLA) (50 microg/kg per min), to avoid endothelial P2 rec

15 oxide (NO) inhibition with nitro-L-arginine (NLA) or after administration of NO donor agents.

16 odialysis delivery of N(G)-nitro-L-arginine (NLA) significantly reduced ACh release in the cholinergi

17 thetase inhibitor, N omega-nitro-L-arginine (NLA), was investigated in Mongolian gerbils.

18 inhibitor of NO synthase, nitro-L-arginine (NLA, 30 mg/kg i.v.), caused a maintained increase in mea

19 Nitro-L-arginine (NLA, 35 mg/kg IV) was given to block NO synthesis, and t

20 asodilation was blunted by nitro-L-arginine (NLA, 35 mg/kg).

21 of the NOS inhibitor N(G)-nitro-l-arginine (NLA; 10 mm) increased ACh release during wakefulness (33

22 N-nitro-l-arginine [NLA; a nitric oxide synthase (NOS) inhibitor] and l-argi

23 The "2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With C

24 ively known as the nucleotide loop assembly (NLA) pathway.

25 nostic criteria [National Lipid Association (NLA), International Lipid Expert Panel (ILEP), and Europ

26 WT was significantly lower at NLA centers compared with non-NLA centers for top-band p

27 In the archaeal and bacterial NLA pathways, two different guanylyltransferases catalyz

28 by adding a single purification step before NLA:III digestion of the ditags.

29 PHT1s in nla mutants and interaction between NLA and PHT1s in the plasma membranes suggests that NLA

30 on is increased with exercise and blocked by NLA.

31 ients was no different (P > 0.999) comparing NLA with non-NLA centers.

32 for top-band patients (P > 0.999) comparing NLA with non-NLA centers.

33 sults show that under Pi-replete conditions, NLA and UBC24 target the PT2 transporter for destruction

34 led that among the three sample groups (CTL, NLA and PLS) there were 19 miRNA, including several nove

35 During NLA infusion, the RIHP responses to reductions in RAP we

36 la) motifs in most aquaporins, the PbAQP has NLA (Asn-Leu-Ala) and NPS (Asn-Leu-Ser) in those positio

37 naling/homeostasis regulation by identifying NLA and UBC24 as partners and PT2 as one of their downst

38 the late postischemic hypoperfusion seen in NLA-, N omega-nitro-D-arginine methyl ester- or Ringer's

39 Consistent with NLA/UBC24 function, induced NLA expression causes a UBC24-dependent decrease in PT2

40 Intriguingly, NLA and PHO2 are the targets of two Pi starvation-induce

41 m normal-appearing areas, away from lesions (NLA) and from the periphery of lesions- plaque shadow (P

42 p epochs was significantly decreased by mPRF NLA administration.

43 antly lower at NLA centers compared with non-NLA centers for top-band patients (23 versus 99 days, P

44 patients (P > 0.999) comparing NLA with non-NLA centers.

45 different (P > 0.999) comparing NLA with non-NLA centers.

46 fic protease 12/13) antagonize the action of NLA (nitrogen limitation adaptation) E3 ligase to mainta

47 Dialysis administration of NLA did not alter respiratory rate.

48 screens we identified several candidates of NLA-interacting proteins that are involved in a wide ran

49 by overexpression a miR827-resistant cDNA of NLA produced the opposite phenotype of reduced plant sus

50 dence that miR827-mediated downregulation of NLA to suppress basal defense pathways.

51 s that UBP12/UBP13 counteracts the effect of NLA E3 ligase to accelerate leaf senescence under nitrog

52 The different effects of NLA on ACh release in the cat pons and cat basal forebra

53 Loss of function of NLA caused high Pi accumulation resulting from increases

54 Injection of NLA into the mPRF before neostigmine injection also bloc

55 rmore, different subcellular localization of NLA and phosphate2 (pho2; a ubiquitin E2 conjugase) and

56 Microinjection of NLA into the lateral basal forebrain did not significant

57 nts demonstrated that mPRF microinjection of NLA significantly reduced the amount of REM sleep and th

58 During the Pi deprivation response, NLA and PHO2 transcripts are cleaved by miR399 and miR82

59 rs of the Pht1 Pi-transporter family tested, NLA associates only with PT2 (Pht1;4).

60 t pons, the present results demonstrate that NLA increased ACh release in the cat basal forebrain and

61 Here, we show that NLA is an E3 ligase that specifically requires UBC24 for

62 PHT1s in the plasma membranes suggests that NLA directs the ubiquitination of plasma membrane-locali

63 The NLA achieved its aim, providing earlier transplantation

64 The NLA-UBC24 pair mediates polyubiquitination of PT2 but no

65 Meanwhile, the NLA target gene, which encodes an ubiquitin E3 ligase en

66 We investigated whether the NLA had improved WL survival and waiting time (WT) to tr

67 5 microg/kg per min) administration in these NLA-treated dogs decreased RBF (2.5+/-0.3 ml/min per g;

68 ATP administration to NLA-treated dogs resulted in further decreases in RBF (2

69 In contrast to NLA-induced depression of REM sleep and ACh release in t

70 he prevalence was similar when defined using NLA, ILEP, and EAS criteria [7.0% (6.0-8.0%), 6.7% (5.0-

71 Consistent with NLA/UBC24 function, induced NLA expression causes a UBC2

72 red metabolites and miRNA comparing CTL with NLA and NLA with PLS, identified several hubs of metabol

73 ecovery of cerebral blood flow observed with NLA without affecting the late postischemic hypoperfusio