ライフサイエンスコーパス: mitochondrial K(ATP) channel

1 d to assess the potential involvement of the mitochondrial KATP channel.

2 re or is mediated via the sarcolemmal or the mitochondrial KATP channel.

3 a KATP channel opener, selectively activates mitochondrial KATP channels.

4 ators that activate both plasma membrane and mitochondrial KATP channels.

5 tconditioning, indicating involvement of the mitochondrial K(ATP) channel.

6 ypoxia from birth alters the function of the mitochondrial K(ATP) channel.

7 t ischemia/reperfusion injury via opening of mitochondrial K(ATP) channels.

8 , production of nitric oxide, and opening of mitochondrial K(ATP) channels.

9 ibly through protein kinase G and opening of mitochondrial K(ATP) channels.

10 id delta(1) receptors leads to activation of mitochondrial K(ATP) channels.

11 n afforded by diazoxide (Diaz), an opener of mitochondrial K(ATP) channels.

12 normoxic heart mitochondria consistent with mitochondrial K(ATP) channel activation and mitochondria

13 effects of adenosine and diazoxide reflected mitochondrial K(ATP) channel activation, because they co

14 ction from both ischemic preconditioning and mitochondrial KATP channel activation.

15 ac myocytes and is most likely the result of mitochondrial KATP channel activation.

16 ective effect that is possibly the result of mitochondrial KATP channel activation.

17 Adenosine (100 micromol/L) increased mitochondrial K(ATP) channel activity and abbreviated th

18 zoxide (100 micromol/L) was used to quantify mitochondrial K(ATP) channel activity in intact rabbit v

19 ity transition pore, to ion channels such as mitochondrial K(ATP) channels and connexin-43 have now b

20 These results show that opening of mitochondrial K(ATP) channels and generation of reactive

21 ection by a pathway that requires opening of mitochondrial K(ATP) channels and production of free rad

22 oteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator

23 clude protection against ischaemic injury by mitochondrial KATP channels and the contribution of inne

24 er glibenclamide or the putatively selective mitochondrial K(ATP) channel antagonist 5-hydroxydecanoa

25 droxydecanoate (100 micromol/L), a selective mitochondrial K(ATP) channel antagonist.

26 a low dose of the protonophore FCCP, or the mitochondrial KATP channel antagonist, tolbutamide.

27 We conclude that mitochondrial K(ATP) channels are activated in chronical

28 The biochemical properties of the mitochondrial KATP channel are very similar to those of

29 hannel openers, raising the question whether mitochondrial KATP channels are similarly sensitive to t

30 blockade (glibenclamide or HMR 1098) but not mitochondrial K(ATP) channel blockade (5-hydroxydecanoat

31 vation, because they could be blocked by the mitochondrial K(ATP) channel blocker 5-hydroxydecanoate

32 In contrast, 5-hydroxydecanoate, a mitochondrial KATP-channel blocker, was ineffective, as

33 otein kinase C antagonist chelerythrine, and mitochondrial K(ATP) channel closer 5-hydroxydecanoate e

34 A quantitative model of mitochondrial K(ATP) channel gating reproduced the major

35 ne receptor activation primes the opening of mitochondrial K(ATP) channels in a protein kinase C-depe

36 s for an involvement of both sarcolemmal and mitochondrial K(ATP) channels in such protection.

37 nd 5-hydroxydecanoic acid, selective for the mitochondrial KATP channel in rabbits.

38 We suggest that the mitochondrial KATP channel is an important intracellular

39 We propose that the open-closed state of the mitochondrial KATP channel is determined by the relative

40 not sarcolemmal KATP channels and imply that mitochondrial KATP channels may mediate the protection f

41 dence suggested that the recently identified mitochondrial KATP channel (mito KATP) may be the potass

42 lyl cyclase, protein kinase G (PKG), and the mitochondrial K(ATP) channel (mitoK(ATP)).

43 The mitochondrial KATP channel (mitoKATP) is highly sensitiv

44 The mitochondrial KATP channel (mitoKATP) is hypothesized to

45 Activated PKG opens mitochondrial KATP channels (mitoKATP) which increase pr

46 However, 5-hydroxydecanoate and diazoxide- mitochondrial K(ATP) channel modulators-did not affect N

47 ether or alone with and without diazoxide, a mitochondrial K(ATP) channel opener.

48 econditioning (IP), presumably by inhibiting mitochondrial K(ATP) channel opening in myocytes.

49 lim does not block the beneficial effects of mitochondrial K(ATP) channel opening in the isolated rat

50 nnel activity and abbreviated the latency to mitochondrial K(ATP) channel opening.

51 lude that this pathway is not related to the mitochondrial KATP channel or the Ca2+-dependent permeab

52 Moreover, blocking mitochondrial K(ATP) channels removed preconditioning be