ライフサイエンスコーパス: CPK

1 CPK-MB concentrations were determined in 15 of 18 patien

2 CPKs are composed of a dual specificity (Ser/Thr and Tyr

3 Based on their dependence on Ca(2+), CPKs can be sorted into three types: strictly Ca(2+)-dep

4 2+) activation to a biological function of a CPK.

5 SGOT, LDH, ALP, and CPK levels on POD 1 were elevated above baseline in all

6 We characterized anion channels and CPK transcripts in PTs and analyzed their localization.

7 or 70 micromol choline/L for up to 96 h, and CPK was measured in the media; choline and metabolites w

8 pancreatic lesions that developed in KPC and CPK mice expressed TIMP1 and secreted it into the circul

9 al infarctions (signified by new Q waves and CPK-MB >8xULN) are powerful determinants of death, where

10 bution of autophosphorylation in controlling CPK activity is less well understood.

11 Nitrate-coupled CPK signalling phosphorylates conserved NIN-LIKE PROTEIN

12 rin, but it was only slightly affected by CP/CPK, ARL-66096, or A3P5PS.

13 reatine phosphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of the ADP P2T(AC) re

14 into three types: strictly Ca(2+)-dependent CPKs, Ca(2+)-stimulated CPKs (with a significant basal a

15 of the disease, the later onset of elevated CPK and eosinophilia, and the possibility for relapses.

16 ase LDL cholesterol level without increasing CPK or pain levels and may be a treatment option for dys

17 and significantly decreased ischemia-induced CPK release and infarct size.

18 Ca(2+)), and essentially calcium-insensitive CPKs.

19 egulates a CDPK, a recombinant CDPK (isoform CPK-1 from Arabidopsis, accession no. L14771) was made a

20 Release of creatine phosphate kinase (CPK) in the samples of coronary effluent and infarct siz

21 subgroup III Ca(2+)-sensor protein kinases (CPKs) as master regulators that orchestrate primary nitr

22 Ca(2+)-dependent protein kinases (CPKs) decode the Ca(2+) signal, also facilitating defens

23 Ca(2) (+)-dependent protein kinases (CPKs) form a large family of 34 genes in Arabidopsis (Ar

24 calcium (Ca(2+))-dependent protein kinases (CPKs) represent the primary Ca(2+)-dependent protein kin

25 ity of two Ca(2+)-dependent protein kinases (CPKs), isoforms CPK17 and -34.

26 resence of Ca(2+)-dependent protein kinases (CPKs).

27 As expected from Corey-Pauling-Koltun (CPK) models, the cryptand with the tri(ethyleneoxy) arm

28 tf1a(+)/Cre;Kras(+)/LSL-G12D;Trp53loxP/loxP (CPK) mice, Pdx-1(+)/Cre;Kras(+)/LSL-G12D;Trp53(+)/LSL-R1

29 ficient medium for 72 h leaked 3.5-fold more CPK than did cells grown in medium with 70 micromol chol

30 survival was unaffected by lesser degrees of CPK-MB elevation.

31 rminants of death, whereas lesser degrees of CPK-MB release and specific device use do not adversely

32 fragile and results in increased leakage of CPK from cells.

33 was no relationship between the magnitude of CPK-MB concentrations and the terbutaline or epinephrine

34 as collected at intervals for measurement of CPK.

35 No difference in the risk of CPK elevation was observed between the treatment groups

36 Here, we report on the third type of CPK, CPK13, which is expressed in guard cells but whose

37 Although regulation of CPKs by Ca(2+) has been extensively studied, the contrib

38 cholesterol, triglyceride, liver enzyme, or CPK; weight loss; and pain severity scores did not signi

39 The peak periprocedural CPK-MB level was >3x the upper limit of normal (ULN) in

40 in the muscle enzyme creatine phosphokinase (CPK) 4 weeks after gene transfer.

41 s and the release of creatine phosphokinase (CPK) as a sequela of that deficiency.

42 gical clearance, and creatine phosphokinase (CPK) elevation.

43 Serial creatine phosphokinase (CPK)-MB levels were determined after elective percutaneo

44 and elevated serum creatinine phosphokinase (CPK) levels were observed beginning during the fifth wee

45 liver enzyme, and creatinine phosphokinase (CPK) levels; weight; and Brief Pain Inventory score.

46 ogenase (LDH), and creatinine phosphokinase (CPK).

47 We therefore screened a subset of plant CPKs for CaM binding and found that CPK28 is a high affi

48 We propose CPK as the gene designation for this family of enzymes a

49 sive with folding of the central pseudoknot (CPK), a universally conserved rRNA structure of the smal

50 Serum CPK may be a useful clinical marker for choline deficien

51 pients, and graft injury determined by serum CPK-MB levels was significantly decreased.

52 icient diet had significantly elevated serum CPK activity derived from skeletal muscle (up to 66-fold

53 mini are phosphorylated by a pollen-specific CPK that modifies their water permeability.

54 tly Ca(2+)-dependent CPKs, Ca(2+)-stimulated CPKs (with a significant basal activity in the absence o

55 these results provide genetic evidence that CPKs are essential to pollen fitness, and support a mech

56 (PBMCs) from the subject who experienced the CPK elevation showed the activation of capsid-specific C

57 o the pre-rRNA including those that form the CPK.

58 binds PtdIns-3-P, while the PX domain of the CPK PI-3 kinase selectively binds PtdIns-4,5-P(2).

59 owever, there as yet is no equivalent of the CPK-MB for acute myocardial infarction.

60 omal proteins (r-proteins) that surround the CPK.

61 Though CPK-MB elevation was more common after atheroablation an

62 ore, whether calmodulin (CaM) contributes to CPK regulation, as is the case for Ca(2+)/CaM-dependent

63 ent from F436 to I444 (numbers correspond to CPK-1 accession number L14771).

64 Non-Q-wave MI with CPK-MB >8x ULN was also a strong predictor of death (2-y

65 for a T-DNA insertion that was found within CPK-9, a member of the gene family encoding calmodulin-d