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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 on is increased with exercise and blocked by NLA.

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

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

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

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

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

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

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

33 p epochs was significantly decreased by mPRF NLA administration.

34 Dialysis administration of NLA did not alter respiratory rate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 5 microg/kg per min) administration in these NLA-treated dogs decreased RBF (2.5+/-0.3 ml/min per g;

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

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

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

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