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1 ere modeled in the C terminus of muscle-type creatine kinase.
2 pyruvate kinase muscle isozyme, isoforms of creatine kinase.
3 pomyosin, myosin or an isoform of the enzyme creatine kinase.
4 d pathology and reduction in levels of serum creatine kinase.
5 ors make neurotransmission less dependent on creatine kinase.
6 ith significant reduction in levels of serum creatine kinase.
7 ins such as myosin heavy chain fast type and creatine kinase.
8 roximal weakness and markedly elevated serum creatine kinase.
9 kinase and 427 with only the MB fraction of creatine kinase.
10 causing pain or cramping or increasing serum creatine kinase.
11 ficulties, and normal to moderately elevated creatine kinase.
12 aminotransferase, lactate dehydrogenase, and creatine kinase.
13 thesis from OXPHOS, anaerobic glycolysis and creatine kinase.
14 assessed by cardiac enzymes, troponin I, and creatine kinase.
15 table for bulky ASB9 substrates, such as the creatine kinases.
16 ut preinfarction angina (n=166) by both peak creatine kinase (1094+/-75 IU/L versus 2270+/-102 IU/L;
17 d in 9 healthy men (mean age 27.9 y, SE 3.3; creatine kinase 115 to 859 IU/L, median 358), was associ
20 fat, cold exposure stimulates mitochondrial creatine kinase activity and induces coordinated express
21 further explore the effect of calmodulin on creatine kinase activity and show that it is increased b
23 imus lumborum and a 5-fold increase in serum creatine kinase activity compared with healthy male litt
24 on and reduced the vascular adenylate kinase/creatine kinase activity ratio essential for the respons
25 l muscle health in mdx mice, reducing plasma creatine kinase activity, an established measure of musc
26 on of inflammatory markers of muscle damage (creatine kinase activity, C-reactive protein, proinflamm
27 e, as evidenced by i) normal levels of serum creatine kinase activity, ii) a lack of Evans blue dye u
31 lar to enolase, pyruvate kinase, isoforms of creatine kinase, aldolase A and an isoform of glyceralde
32 nin, 538 MIs were identified versus 327 with creatine kinase and 427 with only the MB fraction of cre
33 ease above the number of MIs identified with creatine kinase and a 41% (95% CI, 37% to 46%) increase
34 ne blood chemistry was normal, as were serum creatine kinase and aldolase levels and thyroid, hepatic
35 ngs to the phosphagen kinase family of which creatine kinase and arginine kinase are the typical repr
38 ult onset muscular dystrophy with high serum creatine kinase and that mutation screening, particularl
39 rast-enhanced cardiac MRI (CMRI; day 3+/-1), creatine kinase and troponin I area-under-the-curve, and
42 ervations of immobilization of mitochondrial creatine kinase and type I hexokinase on biological memb
43 derived from lactate dehydrogenase, one from creatine kinase, and four from serum albumin protein.
44 , Minnesota coding of the ECG, and troponin, creatine kinase, and its MB fraction measured simultaneo
46 ge, sex, and admission levels of troponin I, creatine kinase, and N-terminal pro-brain natriuretic pe
47 f such therapy, the levels of troponin T and creatine kinase, and the rates of bleeding and stroke di
48 5 IU/L versus 2270+/-102 IU/L; P<0.0001) and creatine kinase area under curve (18 420+/-18 941 versus
49 terquartile range, 14-42; P<0.01) and median creatine kinase areas under the curve were 22 000 and 38
50 with serum muscle enzyme levels (P<0.05 for creatine kinase, aspartate aminotransferase, and aldolas
51 variability compared with the commonly used creatine kinase assay, and correlated better with the re
52 revealed that they have close similarity to creatine kinase B (CKB) isoforms, heterogeneous nuclear
54 e levels of creatine kinase, MB isoenzyme of creatine kinase, blood urea nitrogen, creatinine, K(+) i
55 sed guanidinoacetate N-methyltransferase and creatine kinase, both at the protein and RNA levels, and
58 ce of isotopically enriched magnesium on the creatine kinase catalyzed phosphorylation of adenosine d
59 ription, and QI 3 = complete blood count and creatine kinase check every 6 months for gout patients r
60 s critical role in hair bundle function, the creatine kinase circuit is essential for high-sensitivit
64 after exposure to in vitro oxidative stress: creatine kinase (CK) and glyceraldehyde-3-phosphate dehy
66 kinases of known structure (the homodimeric creatine kinase (CK) and the monomeric arginine kinase (
69 utilization networks in response to chronic creatine kinase (CK) deficiency, a hallmark of cardiovas
71 f the absolute level and rate of increase of creatine kinase (CK) elevation after primary percutaneou
73 describe an imaging method that employs the creatine kinase (CK) gene as a marker of donor hepatocyt
76 n the anti-Jo-1 antibody level and the serum creatine kinase (CK) level, as well as muscle and joint
78 a 2-tiered approach to NBS with screening by creatine kinase (CK) levels in dried blood spots followe
82 ovascular death or nonfatal MI, defined as a creatine kinase (CK) MB fraction of at least 100 ng/mL o
84 iation of a recently reported variant in the creatine kinase (CK) muscle gene, CKM Glu83Gly (rs115590
85 ATP production rate constants (k(f)) through creatine kinase (CK) or ATP synthase (ATPase) with 2 spe
89 lationship between cTnT, cardiac troponin I, creatine kinase (CK), CK-myocardial band levels, and ske
90 tions, and measurements of serum cTnT, cTnI, creatine kinase (CK), creatine kinase myocardial band (C
92 a showing reduced metabolism through cardiac creatine kinase (CK), the major myocardial energy reserv
93 enosine triphosphate (ATP) synthesis through creatine kinase (CK), the primary myocardial energy rese
94 or decreased intracellular ATP generation by creatine kinase (CK), the prime energy reserve of the he
96 Creatine treatment enhanced cell fusion in a creatine kinase (CK)-dependent manner suggesting that AT
98 defined as: 1) new Q-wave and MB isoform of creatine kinase (CK-MB) elevation (daily electrocardiogr
100 ir of high-energy phosphate (HEP) bonds, and creatine kinases (CK) catalyze the transfer of HEP from
101 Gower score, time to run 30 feet, and serum creatine kinase [CK] level) and with nonquantitative MR
102 s, we identified that brain-type cytoplasmic creatine kinase (Ckb) was greatly induced in mature oste
103 identified the ATP-buffering, mitochondrial creatine kinase CKMT1 as necessary for survival of EVI1-
105 e dye uptake into muscle and increased serum creatine kinase compared to the 129T2/SvEmsJ background.
106 he most common adverse event was an elevated creatine kinase concentration to more than ten times the
107 ical and functional changes using the muscle creatine kinase conditional frataxin knockout (KO) mouse
108 Ablation of Vps34 in the heart of muscle creatine kinase-Cre;Vps34(f/f) mice led to cardiomegaly
110 mechanical overload, which decreased muscle creatine kinase-driven TEAD-1 transgene expression, and
112 on and the contribution of other isoforms of creatine kinase during RANKL-induced osteoclastogenesis
113 different than control in terms of myalgia, creatine kinase elevation, cancer, and discontinuations
115 tin at its highest doses was associated with creatine kinase elevations (odds ratio, 4.14; 95% credib
116 00 patients [RD], 2.7; 95% CI, -3.2 to 8.7), creatine kinase elevations (RD, 0.2; 95% CI, -0.6 to 0.9
117 omyolysis is rare, muscle symptoms and serum creatine kinase elevations are sufficiently frequent dur
118 ransaminase elevations, but not of myalgias, creatine kinase elevations, rhabdomyolysis, or withdrawa
119 rapy versus placebo; and reports of myalgia, creatine kinase elevations, rhabdomyolysis, transaminase
123 (STOMP) study assessed symptoms and measured creatine kinase, exercise capacity, and muscle strength
124 3 and miR-551a expression, which derepresses creatine kinase expression and allows energy to be captu
126 common grade 3-4 adverse events were raised creatine kinase (five [6%] in the 200 mg group vs 19 [13
127 ne kinase reaction, we have now measured the creatine kinase forward reaction rate constant in BD.
129 hy control participants at 4T and quantified creatine kinase forward reaction rate constant using (31
130 ants or isoforms of tropomyosin, arginine or creatine kinase, glyceraldehyde-3-phosphate dehydrogenas
131 R, 2.620; 95% CI, 1.073-6.399; P = .035) and creatine kinase (>800 U/L; OR, 2.328; 95% CI, 1.129-4.80
133 Consistent with this model, inhibition of creatine kinase in avascular retinas blocks synaptic tra
134 on by OXPHOS (vOX), anaerobic glycolysis and creatine kinase in moderate and severe intensity exercis
135 here was a significant increase in mean peak creatine kinase in the oxygen group compared with the no
136 value exceeded 10 times normal, but average creatine kinase increased 20.8+/-141.1 U/L (P<0.0001) wi
137 ant bundle protein; at approximately 0.5 mM, creatine kinase is capable of maintaining high ATP level
148 = 0.45; I2 = 0%), and increases in the serum creatine kinase level were reduced (OR, 0.72 [CI, 0.54 t
150 ntractures, severe scoliosis, elevated serum creatine kinase level, myopathic electrodiagnostic chang
152 ecificity had proximal weakness (100%), high creatine kinase levels (mean maximum 10,333 IU/liter), a
154 d by adult onset muscle weakness, high serum creatine kinase levels and a prominent inflammatory infi
159 Myopathy--muscle pain or weakness with blood creatine kinase levels more than ten times the upper lim
160 ociated with an increased incidence of serum creatine kinase levels that were more than 10 times the
161 ntral nucleation, tissue fibrosis, and serum creatine kinase levels were dramatically reduced in Sgcd
165 thy characterized by mildly increased plasma creatine kinase levels, a variation in myofibre size and
167 distribution and significantly reduced serum creatine kinase levels, but had limited effect on muscle
168 of Dmdmdx-5Cv mice results in reduced serum creatine kinase levels, improved sarcolemmal integrity,
169 ake, increased muscle fibre necrosis, plasma creatine kinase levels, muscle PDK4, muscle atrophy F-bo
170 is was associated with greatly reduced serum creatine kinase levels, near-normal histology, and funct
185 globin and somatic cytochrome-C) and others (creatine kinase M, malate dehydrogenase cytosolic, fibri
186 Fractional synthesis rate (FSR) of plasma creatine kinase M-type (CK-M) and carbonic anhydrase 3 (
188 protein expression of creatine kinase-mt and creatine kinase-m isoforms was significantly reduced in
190 ved hemodynamics and decreased the levels of creatine kinase, MB isoenzyme of creatine kinase, blood
191 similar or lower in HBOC than HEX pigs, but creatine kinase-MB (but not creatine kinase-MB/creatine
194 (TnI), B-type natriuretic peptide (BNP), and creatine kinase-MB (CK-MB), and TnI and BNP by CART.
195 similar information as a value of 5x ULN for creatine kinase-MB (hazard ratio, 4.31; 99% confidence i
197 l-resistant patients had higher incidence of creatine kinase-MB elevation than the respective sensiti
199 re hemodynamic deterioration, preangiography creatine kinase-MB isoenzyme rise >2 x normal, and time
200 (cardiac troponin I level > or =0.7 ng/mL or creatine kinase-MB level > or =5.0 ng/mL and/or diagnost
201 images provided equal performance, and peak creatine kinase-MB levels correlated with MRI infarct si
206 43; P=0.003 and hazard ratio per doubling of creatine kinase-MB, 1.30; 95% confidence interval, 1.05-
207 ity C-reactive protein (hs-CRP), Troponin-T, creatine kinase-MB, fibrinogen, and D-Dimer concentratio
211 an HEX pigs, but creatine kinase-MB (but not creatine kinase-MB/creatine kinase ratio) was higher wit
212 function, and perfusion), injury biomarkers (creatine-kinase-MB and troponin I), and histopathologic
214 inol-binding protein (hRBP) under the muscle creatine kinase (MCK) promoter (MCKhRBP) with the PKCdel
215 ified a conserved sequence within the Muscle creatine kinase (MCK) promoter that is critical for high
219 (ACh) receptor (alpha-AChR), desmin, muscle creatine kinase (MCK), myosin heavy chain (MHC) isoforms
220 ke signaling in this process, we used muscle creatine kinase (MCK)-Cre to disrupt expression of insul
221 omatic gene transfer or transgenesis (muscle creatine kinase [MCK]-EcSOD) in mice significantly atten
222 -activated receptor alpha (PPARalpha; muscle creatine kinase [MCK]-PPARalpha) or PPARbeta/delta (MCK-
223 on of the tyrosine phosphatase SHP-2 (muscle creatine kinase [MCK]-SHP-2 null) exhibited a reduction
224 5:00 am onset of reperfusion, with the peak creatine kinase measured at the peak of the curve being
225 n of total reverse T3, high concentration of creatine kinase, mild anaemia), and radiological (thicke
226 st notably the regions harboring CKMT2 gene (creatine kinase, mitochondrial 2) and RASGRF2 gene (Ras
227 ltiplexed detection of 100 fg/ml troponin T, creatine kinase MM, and creatine kinase MB in serum.
230 ts, there was a reduction in serum levels of creatine kinase muscle-brain isoenzyme, a myocardial-spe
231 Prespecified secondary outcome measures of creatine kinase, muscle strength and function, motor ner
232 s of serum cTnT, cTnI, creatine kinase (CK), creatine kinase myocardial band (CK-MB), and N-terminal
235 ention (PCI, procedural MI) using increasing creatine kinase-myocardial band (CK-MB) thresholds with
238 ethodology to assess the association between creatine kinase-myocardial band and 1-year mortality.
241 High-sensitivity cardiac troponin T and creatine kinase-myocardial band were measured before and
243 me parameter was the area under the curve of creatine kinase-myocardial brain fraction concentration.
245 arkers included high-sensitivity troponin T, creatine kinase, myoglobin, N-terminal B-type natriureti
246 n evident by a decrease in the expression of creatine kinase, myosin heavy chain-fast twitch, myogeni
247 o proceeded directly to phase B for elevated creatine kinase (N = 218, with 73 randomized to ezetimib
248 h large increases in blood concentrations of creatine kinase), new-onset diabetes mellitus, and, prob
252 nfarction </=1 flow, there was reduced serum creatine kinase (P=0.030) and a 19% reduction in cardiac
253 rapid ATP generation via the phosphocreatine-creatine kinase (PCr/CK) system, as a unique gene family
254 7 g/m(2) vs. 21 +/- 14 g/m(2); p = 0.01) and creatine kinase peak serum level (median [interquartile
255 Structural analysis of modified muscle-type creatine kinase peptide variants by two-dimensional NMR
256 letal muscle under the control of the muscle creatine kinase promoter (MCKcre mice) with mice having
257 e overexpressing PGC-1alpha under the muscle creatine kinase promoter (MPGC-1alphaTG mice) displayed
260 d reporter genes, including the myogenin and creatine kinase promoters, and by complete inhibition of
261 conversion of phosphocreatine to creatine by creatine kinase provides an essential chemical energy so
262 eatine kinase-MB (but not creatine kinase-MB/creatine kinase ratio) was higher with HBOC in moderate
264 muscle anaerobic metabolism, the rate of the creatine kinase reaction, intracellular buffering of pro
265 is replenished from phosphocreatine via the creatine kinase reaction, we have now measured the creat
269 y (31)P nuclear MR spectroscopy, lactate and creatine kinase release spectrophotometrically, and hypo
270 e estimated by peak and area under the curve creatine kinase release was measured in all study popula
271 that the extent of infarct size measured by creatine kinase release was significantly associated wit
274 and increased aspartate aminotransferase and creatine kinase serum enzyme levels in cynomolgus macaqu
275 ed muscle degeneration and fibrosis, reduced creatine kinase serum levels, restored running capacity
277 Diagnosis using the classic blood marker creatine kinase sometimes yields unsatisfactory results
278 the phosphocreatine shuttle, where flagellar creatine kinase (Sp-CK) uses phosphocreatine to rephosph
281 apacity of oxidative phosphorylation and the creatine kinase system to buffer the cellular ATP/ADP ra
282 to examine the bioenergetic reactions of the creatine-kinase system and the ATP synthesis/hydrolysis
283 es, including aspartate aminotransferase and creatine kinase, that are typically elevated as a result
284 We assessed whether the level of plasma creatine kinase, the enzyme that utilizes ADP and phosph
285 , the characteristic clearance properties of creatine kinase, the time course of muscle fiber regener
286 intra- and intermolecular cross-links within creatine kinase, then to map the interaction surfaces be
287 sterol, low-density lipoprotein cholesterol, creatine kinase, thyroid-stimulating hormones, and eryth
289 n, stabilized the sarcolemma, restored serum creatine kinase to wild-type levels, and protected muscl
290 olipoprotein A1 (apoA1), apoE, mitochondrial creatine kinase U-type, beta-synuclein, synaptogyrin-3,
292 lower limb weakness with highly raised serum creatine kinase values (average 4500 IU/l) and frequent
296 r beta-actin, the cytosolic brain isoform of creatine kinase was the next most abundant bundle protei
297 tions of serum transaminases, bilirubin, and creatine kinase were infrequent and similar between grou
298 ion of MyoD-target genes myogenin and muscle creatine kinase were suppressed by PAX3/FOXO1A or PAX7/F
299 erize the interaction between calmodulin and creatine kinase, which we identify as a novel calmodulin
300 tion of myocardial ATP, phosphocreatine, and creatine kinase with decreased efficiency of mechanical
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