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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 tion in either group were increased creatine phosphokinase (52 [19%] of 269 patients in the binimetin
6 tionally rewired via cAMP and cAMP-dependent phosphokinase A (PKA)-mediated activation of the cAMP-re
7 inc supplementation decreased serum creatine phosphokinase activities and eliminated the difference b
11 se factors, which lacked detectable creatine phosphokinase and ATPase activities, creatine phosphate
13 ced an elevation in serum levels of creatine phosphokinase and myocardial injury characterized by the
16 id peroxidation, elevation of serum creatine phosphokinase, and functional changes in the isolated at
17 ase duration, skin score, levels of creatine phosphokinase, and presence of tendon friction rubs.
19 ion and role was examined by immunostaining, phosphokinase antibody arrays, Western blot analysis, an
20 pip92/Ier2/ETR101 does not appear to require phosphokinase C activity for transcriptional activation.
23 3Gly (rs11559024) with constitutive creatine phosphokinase (CK) levels, CK variation, and inducibilit
24 an asymptomatic increase in plasma creatine phosphokinase concentration (200 mg, n=5; 400 mg, n=3; 8
25 n, ADP scavenger creatine phosphate/creative phosphokinase (CP/CPK), and ARL-66096, an antagonist of
29 d eosinophilia and elevated serum creatinine phosphokinase (CPK) levels were observed beginning durin
30 , triglyceride, liver enzyme, and creatinine phosphokinase (CPK) levels; weight; and Brief Pain Inven
33 .1.3); (ii) transferase activity of creatine phosphokinase (EC 2.7.3.2) and hexokinase (EC 2.7.1.1);
34 nt-related adverse events occurred (creatine phosphokinase elevation attributed to antilipid therapy
38 tatin and 7 placebo patients due to creatine phosphokinase elevations; no cases of mild or severe myo
40 atient at 20 mg/kg, increased blood creatine phosphokinase in two patients at 20 mg/kg, and increased
41 acebo and vemurafenib group), blood creatine phosphokinase increase (30 [12%] vs one [<1%]), and alan
43 lymphopenia in two patients, blood creatine phosphokinase increase in one patient, aminotransferase
44 ssociation of elevated troponin and creatine phosphokinase isoenzyme levels with mortality and organ
45 ffects on extrarenal injury (plasma creatine phosphokinase, lactate dehydrogenase, and hematocrit lev
46 ps (all p > 0.05), whereas the peak creatine phosphokinase level was significantly reduced in group 2
47 vity Score (DAS) for juvenile DM, creatinine phosphokinase level, aldolase level, absolute number of
48 Elevated temperature, an elevated creatine phosphokinase level, and autonomic dysfunction led to co
49 wer ejection fractions, higher peak creatine phosphokinase levels (P < .0001), and more diseased vess
50 ecipients tested had elevated serum creatine phosphokinase levels and detectable serum myoglobin.
51 t prominent in patients with peak creatinine phosphokinase levels between 500 and 1,000 mg/dl (86% vs
55 opment of new pathologic Q waves or creatine phosphokinase-MB isoenzyme elevation >8 x upper limits o
56 scle, leading to decreased myosin creatinine phosphokinase (MCK) expression and binding activities.
57 ipts including muscle mitochondrial creatine phosphokinase, muscle glycogen phosphorylase, hexokinase
59 une disorder (n=3), increased blood creatine phosphokinase (n=2), and increased aspartate aminotransf
60 inine phosphokinase, r = 0.76 for creatinine phosphokinase of the muscle band, and r = 0.75 for tropo
61 treatment group B), increased blood creatine phosphokinase (one [1%] vs four [4%]), and hypophosphata
63 ize (p < 0.001), cardiac release of creatine phosphokinase (p < 0.001), and apoptotic cell death (p <
65 were found to contain casein kinase (CK) 2, phosphokinase (PK)C phosphorylation, and N-myristoylatio
66 ng multidetector CT (r = 0.82 for creatinine phosphokinase, r = 0.76 for creatinine phosphokinase of
67 h in myocardial damage, assessed by creatine phosphokinase release, and in endothelial cell and cardi
72 had eye defects or elevated muscle creatine phosphokinase, separating the TMTC3 COB phenotype from t
73 y values, including increased blood creatine phosphokinase (seven [8%]), increased alanine aminotrans
75 re were no significant changes in creatinine phosphokinase, trough cyclosporine levels, or total cycl
77 y, skin score, serum creatinine and creatine phosphokinase values, hypothyroidism, and cardiac involv
78 ared to be normal with exception of creatine phosphokinase, which peaked at 7 days after infection.
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