ライフサイエンスコーパス: butanedione monoxime

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1 ensitive to an inhibitor of myosin function (butanedione monoxime).

2 but these increases were not blocked by 2,3-butanedione monoxime.

3 ction coupling) were estimated by use of 2,3-butanedione monoxime.

4 ytoskeleton, and by the myosin inhibitor 2,3-butanedione monoxime.

5 response was reversibly reduced by 5-mM 2,3-butanedione monoxime, a known cross-bridge inhibitor.

6 n specifically inhibited a slow phase, while butanedione monoxime, a myosin ATPase inhibitor, inhibit

7 al stimulation in the presence of 7.5 mM 2,3-butanedione monoxime, an inhibitor of actin-myosin cross

8 The drug butanedione monoxime, an inhibitor of myosins, blocked t

9 ke tension response was affected by both 2,3-butanedione monoxime and sarcomere length in the same ma

10 d reactivators monoisonitrosoacetone and 2,3-butanedione monoxime and shows potential for further ref

11 ADE, butanedione monoxime, and NP were given for cardioprotec

12 The addition of 3 mm 2,3-butanedione monoxime at pCa 9.0 showed that there was ap

13 ng myosin adenosine triphosphatase using 2,3-butanedione monoxime (BDM) and found that phagocytosis w

14 r outer hair cells (OHCs) while applying 2,3-butanedione monoxime (BDM) by pressure.

15 2,3-Butanedione monoxime (BDM) is widely believed to act as

16 d the effect of the chemical phosphatase 2,3-butanedione monoxime (BDM) on glycine current (IGly) of

17 ogenetically activated eggs treated with 2,3-butanedione monoxime (BDM) undergo a dramatic large-scal

18 sate containing 20 nM dopamine, dopamine+2,3-butanedione monoxime (BDM), a MgATPase-inhibitor, or the

19 e the actions of a chemical phosphatase, 2,3-butanedione monoxime (BDM), on endogenous and expressed

20 The myosin ATPase inhibitor, butanedione monoxime (BDM), reversibly inhibited gliding

21 cal-mechanical uncoupling drugs, such as 2,3-butanedione monoxime (BDM).

22 ose of this investigation was to utilize 2,3-butanedione monoxime (BDM; an inhibitor of contractile a

23 nhibited with 0.5 mM AlF4- or with 30 mM 2,3 butanedione-monoxime (BDM) during measurements of the Ca

24 tors, since treatment with cytochalasin D or butanedione monoxime blocks the streaming motion.

25 ves a carbamidodiacetyl reaction between 2,3-butanedione monoxime (diacetylmonoxime) and the de novo

26 The addition of the neutral oxime 2,3-butanedione monoxime increases the rate of reactivation

27 ilaments (cytochalasin D) and myosin ATPase (butanedione monoxime), indicating that they rely on an a

28 n more about the cardioplegic agent BDM (2,3-butanedione monoxime), its effects on the force-velocity

29 n firm substrates with myosin inhibitors 2,3-butanedione monoxime or KT5926 caused the reduction of b

30 Cross-bridge inhibition (with butanedione monoxime) or augmentation (with 2 deoxy-ATP)

31 ith altered concentrations of phosphate, 2,3-butanedione monoxime, or adenosine triphosphate at a fix

32 tochalasin D, genistein, wortmannin, and 2,3-butanedione monoxime-sensitive pathway and replicated wi

33 hydro-1,4-diazapine, cytochalasin D, and 2,3-butanedione monoxime significantly inhibited (P < 0.05)

34 ference was abolished in the presence of 2,3-butanedione monoxime, suggesting that the basal level of

35 in the presence of the tension inhibitor 2,3-butanedione monoxime suggests that regulatory light chai

36 he myosin cross-bridge (inorganic phosphate, butanedione monoxime, trifluoperazine, and blebbistatin)

37 affect strong crossbridge inhibition by 2,3-butanedione monoxime when near-neighbour thin filament R

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