ライフサイエンスコーパス: phosphokinase

1 oligomycin A, phosphocreatine, and creatine phosphokinase.

2 sessed by measuring the levels of creatinine phosphokinase.

3 doxin, ovalbumin, and rabbit muscle creatine phosphokinase.

4 entified as regulators of phospholipases and phosphokinases.

5 e events (AEs) were increased blood creatine phosphokinase (10.0% with cobimetinib plus atezolizumab

6 anaemia (ten [6%]), increased blood creatine phosphokinase (12 [7%]), and fatigue (eight [4%]).

7 notransferase (4 [6.5%] SAD), and creatinine phosphokinase (2 [3.2%) SAD, 1 [14.3%] MAD) were observe

8 adverse events (AEs) were elevated creatine phosphokinase (24%), diarrhea (8%), and anemia (5%).

9 the control group), increased blood creatine phosphokinase (51 [22%] vs 50 [18%]), and increased alan

10 tion in either group were increased creatine phosphokinase (52 [19%] of 269 patients in the binimetin

11 hair color changes (76%), elevated creatine phosphokinase (56%) and anemia (49%).

12 hypertension (10%), increased blood creatine phosphokinase (9%), and lymphopenia (9%).

13 tionally rewired via cAMP and cAMP-dependent phosphokinase A (PKA)-mediated activation of the cAMP-re

14 sociated with lower succinate and creatinine phosphokinase accumulation, suggesting a protective effe

15 inc supplementation decreased serum creatine phosphokinase activities and eliminated the difference b

16 Serum creatine phosphokinase activity was significantly higher in the a

17 protein has constitutively elevated tyrosine phosphokinase activity.

18 changes, and the increase in serum creatine phosphokinase activity.

19 from grade 0 (preclinical; elevated creatine phosphokinase; all activities normal) to grade 9 (unable

20 se factors, which lacked detectable creatine phosphokinase and ATPase activities, creatine phosphate

21 nduced increases in the activity of creatine phosphokinase and creatine kinase-MB.

22 ced an elevation in serum levels of creatine phosphokinase and myocardial injury characterized by the

23 Phosphokinases and protein tyrosine phosphorylation were

24 The relative phosphorylation of 44 phosphokinases and the relative expression of 35 apoptos

25 abeling, (iii) a reduction in serum creatine phosphokinase, and (iv) improved weight gain.

26 id peroxidation, elevation of serum creatine phosphokinase, and functional changes in the isolated at

27 levels of muscle enzymes (aldolase, creatine phosphokinase, and lactate dehydrogenase).

28 ase duration, skin score, levels of creatine phosphokinase, and presence of tendon friction rubs.

29 count and electrolyte, creatinine, creatine phosphokinase, and troponin T levels were normal.

30 ion and role was examined by immunostaining, phosphokinase antibody arrays, Western blot analysis, an

31 In addition, we used proteome profiler phosphokinase arrays to identify signaling changes in Pr

32 these events were increased blood creatinine phosphokinase but were not accompanied by clinical signs

33 pip92/Ier2/ETR101 does not appear to require phosphokinase C activity for transcriptional activation.

34 Also, mTOR-regulated phosphokinase C epsilon (PKCe) activity induced phosphor

35 Additionally, in 9 pigs, creatine phosphokinase (CK) activity in embolized myocardium was

36 3Gly (rs11559024) with constitutive creatine phosphokinase (CK) levels, CK variation, and inducibilit

37 an asymptomatic increase in plasma creatine phosphokinase concentration (200 mg, n=5; 400 mg, n=3; 8

38 n, ADP scavenger creatine phosphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of

39 sient increase in the muscle enzyme creatine phosphokinase (CPK) 4 weeks after gene transfer.

40 on muscle cells and the release of creatine phosphokinase (CPK) as a sequela of that deficiency.

41 e to microbiological clearance, and creatine phosphokinase (CPK) elevation.

42 d eosinophilia and elevated serum creatinine phosphokinase (CPK) levels were observed beginning durin

43 , triglyceride, liver enzyme, and creatinine phosphokinase (CPK) levels; weight; and Brief Pain Inven

44 Serial creatine phosphokinase (CPK)-MB levels were determined after elec

45 lactate dehydrogenase (LDH), and creatinine phosphokinase (CPK).

46 .1.3); (ii) transferase activity of creatine phosphokinase (EC 2.7.3.2) and hexokinase (EC 2.7.1.1);

47 ing vimseltinib was increased blood creatine phosphokinase (eight [10%] of 83).

48 he upadacitinib group was increased creatine phosphokinase (eight [9%] of 93 patients in the upadacit

49 [4%] of 155 in the placebo group), creatine phosphokinase elevation (15 [4%] vs three [2%]), and acn

50 4 toxicity included asymptomatic creatinine phosphokinase elevation (79.1%), hypophosphatemia (14.0%

51 ash (in two patients) and grade 3 creatinine phosphokinase elevation (in one patient) in those who re

52 (18 [12%] vs 22 [14%] vs 15 [10%]), creatine phosphokinase elevation (nine [6%] vs 13 [8%] vs three [

53 ts were rash (11 [19%] patients), creatinine phosphokinase elevation (six [11%]), hypoalbuminaemia (s

54 nt-related adverse events occurred (creatine phosphokinase elevation attributed to antilipid therapy

55 de 2 or worse diarrhoea, rash, or creatinine phosphokinase elevation).

56 d included asthenia, AST elevation, creatine phosphokinase elevation, and decreased appetite.

57 No cases of creatine phosphokinase elevations > or =10 times upper limit of n

58 t is associated with moderate serum creatine phosphokinase elevations in up to 12% of patients.

59 tatin and 7 placebo patients due to creatine phosphokinase elevations; no cases of mild or severe myo

60 Proteasome proteolytic activities and phosphokinase expression were assessed by using specific

61 worse adverse events were elevated creatine phosphokinase (five [10%]) and maculopapular rash (five

62 ncommon, except for 15 increases in creatine phosphokinase in 14 participants (three participants in

63 atient at 20 mg/kg, increased blood creatine phosphokinase in two patients at 20 mg/kg, and increased

64 acebo and vemurafenib group), blood creatine phosphokinase increase (30 [12%] vs one [<1%]), and alan

65 Grade 4 toxicities included creatinine phosphokinase increase (four patients), arterial injury

66 lymphopenia in two patients, blood creatine phosphokinase increase in one patient, aminotransferase

67 occurred in one (2%) patient (blood creatine phosphokinase increase); no fatal events were recorded.

68 (15 [25%] of 60 patients) and blood creatine phosphokinase increased (11 [18%]).

69 n the atezolizumab group were blood creatine phosphokinase increased (123 [53%] of 231 patients), dia

70 (157 [56%] of 280 patients), blood creatine phosphokinase increased (135 [48%]), and rash (119 [43%]

71 mab and control groups were blood creatinine phosphokinase increased (51.3% vs 44.8%), diarrhoea (42.

72 (15 [25%] of 60 patients) and blood creatine phosphokinase increased (ten [17%]).

73 mon being rash (80%, n = 24), blood creatine phosphokinase increased, diarrhea, and nausea (30%, n =

74 ssociation of elevated troponin and creatine phosphokinase isoenzyme levels with mortality and organ

75 ffects on extrarenal injury (plasma creatine phosphokinase, lactate dehydrogenase, and hematocrit lev

76 IGO) stage at admission and serum creatinine phosphokinase level (area under the curve, 0.750; 95% CI

77 njury, and the median (IQR) serum creatinine phosphokinase level was 15 555 (9386-59 274) IU/L.

78 ps (all p > 0.05), whereas the peak creatine phosphokinase level was significantly reduced in group 2

79 vity Score (DAS) for juvenile DM, creatinine phosphokinase level, aldolase level, absolute number of

80 Elevated temperature, an elevated creatine phosphokinase level, and autonomic dysfunction led to co

81 ea; an asymptomatic increase in the creatine phosphokinase level; acneiform rash; and paronychia.

82 e acne (16%), followed by increased creatine phosphokinase levels (13%) and increased lipids (12%).

83 and 11 [4%] patients), elevation in creatine phosphokinase levels (16 [6%] patients, 16 [6%] patients

84 wer ejection fractions, higher peak creatine phosphokinase levels (P < .0001), and more diseased vess

85 ecipients tested had elevated serum creatine phosphokinase levels and detectable serum myoglobin.

86 t prominent in patients with peak creatinine phosphokinase levels between 500 and 1,000 mg/dl (86% vs

87 Examination of serum creatine phosphokinase levels in these mice revealed significant

88 on, oral herpes, elevation of blood creatine phosphokinase levels, headache, and atopic dermatitis.

89 as associated with elevated serum creatinine phosphokinase levels.

90 Creatinine phosphokinase, liver enzyme serum levels, and renal func

91 in serum urea, creatinine, cardiac creatine phosphokinase-MB (CK-MB), and LDH levels.

92 Creatine phosphokinase-MB bands, troponin levels, and pulmonary w

93 opment of new pathologic Q waves or creatine phosphokinase-MB isoenzyme elevation >8 x upper limits o

94 scle, leading to decreased myosin creatinine phosphokinase (MCK) expression and binding activities.

95 ipts including muscle mitochondrial creatine phosphokinase, muscle glycogen phosphorylase, hexokinase

96 Creatinine phosphokinase myocardial band fractions were not signifi

97 twice a day) and grade 4 increased creatine phosphokinase (n = 1; 150 mg once daily).

98 une disorder (n=3), increased blood creatine phosphokinase (n=2), and increased aspartate aminotransf

99 inine phosphokinase, r = 0.76 for creatinine phosphokinase of the muscle band, and r = 0.75 for tropo

100 treatment group B), increased blood creatine phosphokinase (one [1%] vs four [4%]), and hypophosphata

101 e, diabetes, smoking history, serum creatine phosphokinase, or electrocardiographic findings.

102 ize (p < 0.001), cardiac release of creatine phosphokinase (p < 0.001), and apoptotic cell death (p <

103 ibrate, but not LY518674, increased creatine phosphokinase (P = .004 vs placebo).

104 were found to contain casein kinase (CK) 2, phosphokinase (PK)C phosphorylation, and N-myristoylatio

105 ng multidetector CT (r = 0.82 for creatinine phosphokinase, r = 0.76 for creatinine phosphokinase of

106 h in myocardial damage, assessed by creatine phosphokinase release, and in endothelial cell and cardi

107 oved cardiac function and decreased creatine phosphokinase release.

108 oved cardiac function and decreased creatine phosphokinase release.

109 ssment of lactate dehydrogenase and creatine phosphokinase release.

110 On the basis of the results of phosphokinase screening arrays, we here investigate the

111 had eye defects or elevated muscle creatine phosphokinase, separating the TMTC3 COB phenotype from t

112 y values, including increased blood creatine phosphokinase (seven [8%]), increased alanine aminotrans

113 ork that traverses AP-1-activating and other phosphokinase signaling cascades.

114 We tested these fusion proteins in various phosphokinase signaling pathways or cell physiologic ass

115 rminal kinase 1/2/3, Lyn, STAT-3, and STAT-6 phosphokinase signaling.

116 re were no significant changes in creatinine phosphokinase, trough cyclosporine levels, or total cycl

117 Creatine phosphokinase values were monitored and increased above

118 y, skin score, serum creatinine and creatine phosphokinase values, hypothyroidism, and cardiac involv

119 abdominal pain, and increased blood creatine phosphokinase were more frequent with teriflunomide than

120 ared to be normal with exception of creatine phosphokinase, which peaked at 7 days after infection.