ライフサイエンスコーパス: CK

1 CK clustering profiles were indicative of additional zea

2 CK levels >5000 U/L were observed in 36% of patients wit

3 CK values from patients with confirmed EVD were compared

4 CK Vulpeculae was observed in outburst in 1670-1672, but

5 CK was significantly increased in serum compared to othe

6 CK-2066260 has no effect on free cytosolic [Ca(2)(+) ] d

7 CK-2066260 induced a slowing of relaxation, which was ma

8 CK-2066260 treatment also increased skeletal muscle fati

9 CK-2066260 treatment improved in-vivo exercise capacity

10 CK-induced gene expression is partially compromised in L

11 emistry optimization such as olesoxime (11), CK-2127107, RG7800, LMI070, and RG3039 (17).

12 aminotransaminase [ALT] and cytokeratin-18 [CK-18]).

13 rence, 11.9% [95% CI, 9.6% to 14.2%]; Step 2 CK, 85.5% [349/408] vs 95.4% [70,476/73,866]; difference

14 oach was successfully applied to quantify 32 CKs in several biological samples.

15 A CK pretreatment reduced the NF induction of the EARLY NO

16 sions with the MtCRE1 CK receptor gene and a CK response reporter (TWO COMPONENT SIGNALING SENSOR NEW

17 Our results revealed the presence of a CK gradient within the Arabidopsis root tip, with a conc

18 NODULIN11 (ENOD11) symbiotic marker, while a CK-degrading enzyme (CYTOKININ OXIDASE/DEHYDROGENASE3) e

19 effects of compounds that directly activate (CK-1827452) or inhibit (MYK-461) myosin molecules or ind

20 w that the fast skeletal troponin activator, CK-2066260, counteracts muscle weakness by increasing tr

21 biopsy) were analyzed for CK total activity, CK isoforms, citrate synthase activity, and total creati

22 Methylene Blue accumulation in the bud after CK treatment in the dark.

23 ic gross cystic disease fluid protein-15 and CK 7-positive tonofilaments in the pale acinar cells by

24 pared to the high fertilizer rate (53%), and CK (90%).

25 ication of two ARP2/3 inhibitors, CK-548 and CK-666, blocks VE-cadherin dynamics and causes intercell

26 ectroscopy to assess phosphocreatine/ATP and CK kinetics, at rest and during dobutamine stress.

27 thesis and the interaction between auxin and CK are still unclear.

28 lute activities of mitochondrial-type CK and CK-MM isoforms were also lower (P<0.02, all analyses).

29 versible myopathies normalized cTnT, CK, and CK-MB in unison.

30 njury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK-MB).

31 of prolonged elevation of levels of cTnT and CK-MB, which are only produced 6 h after the onset of ch

32 early nodulation in response to both NF and CK signals critical for this symbiotic interaction.

33 Tau P301S and CK-p25 mice subjected to chronic, daily GENUS from the e

34 mpus, and prefrontal cortex in Tau P301S and CK-p25 mouse models of neurodegeneration.

35 e analysis revealed that stem transcript and CK changes were largely associated with decapitation and

36 ing administration of two P2RX7 antagonists (CK, p = 0.030 and p = 0.050) without any detectable side

37 utated CLL lacking CK or TP53abs, as well as CK with +12,+19, show the longest overall survival.

38 genotoxic stress, phosphorylation of the ATM/CK cluster inhibited CREB-mediated gene expression, DNA

39 ATM-independent, phosphorylation of the ATM/CK cluster potentiated bursts in CREB-mediated transcrip

40 a conserved cluster of Ser residues (the ATM/CK cluster) by the DNA damage-activated protein kinase a

41 Creatine kinase-myocardial band (CK-MB) measurements were obtained at baseline and at sev

42 nase and/or creatine kinase-myocardial band (CK-MB) post-procedure were included.

43 d to replicate the association with baseline CK measures.

44 by DELLA1 decreases the amount of bioactive CKs in roots and negatively impacts the Cytokinin Respon

45 ple mutants demonstrates that defects in bud CK response do not affect auxin-mediated bud inhibition,

46 cute pharmacological inhibition of Arp2/3 by CK-666, coupled to quantitative live-cell imaging of the

47 h CKRC1/TAA and CKRC2/YUC8 can be induced by CK and that the phytochrome-interacting factor 4 (PIF4)

48 Transcription of PIF4 itself is induced by CK via the AHKs-ARR1/12 signalling pathway.

49 the respective responses may be mediated by CK signaling, which activates the expression of all six

50 stablished that bud outgrowth is promoted by CK, and that CK synthesis is inhibited by auxin, leading

51 Potentiation of ATP responses by CK and Rd was markedly reduced by mutations S59A, S60A,

52 s, NT5B), C-terminal region of MUC5B (D4-B-C-CK domains, CT5B) and the Cys-domain (within the central

53 T, cardiac troponin I, creatine kinase (CK), CK-myocardial band levels, and skeletal muscle damage wa

54 Here, we report the first comprehensive CK quantification method using a QExactive Orbitrap mass

55 In conclusion, CK-2066260 acts as a fast skeletal troponin activator th

56 tor known to be associated with constitutive CK levels is also associated with CK variability and ind

57 In contrast, CK depletion provoked the coordinated activation of As(V

58 (2) concentration was considered as control (CK).

59 used the spring bare ground as the control (CK).

60 al mastitis (SA group) and healthy controls (CK) were generated by methylated DNA immunoprecipitation

61 e Drosophila unconventional myosin CRINKLED (CK) selectively interacts with the initiator caspase DRO

62 with reversible myopathies normalized cTnT, CK, and CK-MB in unison.

63 marker EpCAM and intracellular cytokeratins (CKs) for isolation and identification, respectively.

64 Auxin and cytokinin (CK) are both important hormones involved in many aspects

65 senescence downstream from auxin, cytokinin (CK), gibberellin (GA), and light signaling.

66 ce between positive regulation by cytokinin (CK) and negative regulation by CLAVATA (CLV).

67 nes involved in the final step of cytokinin (CK) biosynthesis, LONELY GUY3 (LOG3) and LOG4 [8, 9] The

68 ly, early epidermal activation of cytokinin (CK) pathways was indicated, based on the induction of CK

69 berellin signaling and to promote cytokinin (CK) responses, its catalytic OGT activity was never demo

70 Here we use Arabidopsis thaliana cytokinin (CK) biosynthetic and signalling mutants to probe the rol

71 evels of starch in leaves through cytokinin (CK)-regulated processes.

72 Cytokinins (CKs) are adenine derivatives that act as phytohormones.

73 Cytokinins (CKs) play a crucial role in many physiological and devel

74 s severe depletion of endogenous cytokinins (CKs) in the model plant Arabidopsis (Arabidopsis thalian

75 everal plant hormones, including cytokinins (CKs) and gibberellins (GAs).

76 light signaling pathway involve cytokinins (CKs).

77 n of both CUB domains did not prevent VWF D4-CK binding, suggesting that competition for CUB-domain b

78 Both CUB domains could bind to the VWF D4-CK domain fragment (KD of 53.7 +/- 2.1 nm and 84.3 +/- 2

79 an ADAMTS13 activation model in which VWF D4-CK engages the TSP8-CUB2 domains, inducing the conformat

80 eltaTSP8-CUB2 could no longer bind to VWF D4-CK, and deletion of TSP8 abrogated ADAMTS13 conformation

81 pe ADAMTS13 and could be activated by VWF D4-CK.

82 NA]) reveal that, when supplied in darkness, CKs up-regulate their expression as rapidly and as inten

83 This co-culture also led to decreased CK-14 secretion and morphological changes in HMEpiC cell

84 signaling interplays with the CRE1-dependent CK pathway to regulate early nodulation in response to b

85 MTNT can also detect CK-19 mRNA from as few as 2 cancer cells without complic

86 by mutation detection in those with elevated CK.

87 Only large biomarker elevations (CK-MB >=10x upper reference limit and troponin >=70x upp

88 procedures did not greatly alter endogenous CK levels.

89 nd transgenic plants with reduced endogenous CK levels showed an As(V)-tolerant phenotype.

90 xpression phenotypes, including the enhanced CK responses.

91 Myosin, beta-enolase, CK-M-type and actin were identified as main proteins sus

92 iac workload led to an increase in both k(f)(CK) (+86%, P<0.001) and ATP delivery (+80%, P<0.001).

93 ed to no significant increase in either k(f)(CK) (P=0.117) or ATP delivery (P=0.608).

94 In the absence of failure, CK flux was lower in the presence of AS (by 32%, P=0.04)

95 The treatments include no fertilization (CK), low and high manure amendment (M1, M2), chemical ni

96 (types) treatments including no fertilizer (CK), chemical fertilizer (NPK), chemical fertilizer plus

97 % higher than that of the bare fallow field (CK), while the annual CH(4) emissions of the + C treatme

98 ator (ARR) genes increases in buds following CK supply, and that, contrary to their typical action as

99 ssure-loaded heart biopsy) were analyzed for CK total activity, CK isoforms, citrate synthase activit

100 CK signalling, these genes are required for CK-mediated bud activation.

101 onitoring (MRM) methods, previously used for CK profiling on triple quadrupole mass spectrometers.

102 sh, two sRNA libraries derived from Cr-free (CK) and Cr-treated (Cr200) roots were constructed.

103 In conclusion, we show that the FSTA CK-2066260 effectively counteracts muscle fatigue in rod

104 In conclusion, we demonstrate that the FSTA CK-2066260 mitigates skeletal muscle fatigue by reducing

105 st skeletal muscle troponin activator (FSTA) CK-2066260, which increases myofibrillar Ca(2+) sensitiv

106 ule fast skeletal troponin activator (FSTA), CK-2066260, can mitigate muscle fatigue by reducing the

107 C), formerly known as Golgi casein kinase (G-CK), which is exclusively resident in the Golgi apparatu

108 insenoside-F1, highly similar to ginsenoside-CK but containing a single additional hydroxyl group, wa

109 n of ATP-induced cell death with ginsenoside-CK in THP-1 and HEK-hP2X7 cells.

110 Ginsenosides CK and Rd were demonstrated to enhance ATP responses at

111 on of ATP-mediated responses by ginsenosides CK and Rd caused enhanced ionic currents, Ca(2+) influx

112 ction of multiple cardiac biomarkers - GPBB, CK-MB and cTnT for early diagnosis and prognosis of acut

113 ntified at 8, 10, and 1 pg mL(-1), for GPBB, CK-MB and cTnT, respectively, which is well below the cl

114 n the SevAS-reduced ejection fraction group, CK flux was not different from the SevAS-preserved eject

115 One patient had CK level of 9024 U/L and electromyographic study showed

116 In isolated Langendorff-perfused rat hearts, CK inhibition increased ventricular stiffness only in th

117 High-CK with >=5 chromosomal aberrations emerges as prognosti

118 ents with >=5 abnormalities, defined as high-CK, exhibit uniformly dismal clinical outcomes, independ

119 rranted before ultimately incorporating high-CK in risk stratification of CLL.

120 erarchical model in which patients with high-CK exhibit the worst prognosis, whereas those with mutat

121 nsitivity to the hormone and not from higher CK levels.

122 Historically, CK Vul has been considered to be a nova (Nova Vul 1670),

123 Staining for Hmw CKs was also reduced in CRSwNP and CRSsNP, and CK5 mRNA

124 ed in moderate AS and suggest that a fall in CK flux is not by itself a necessary cause of transition

125 Accompanying the fall in CK flux, total CK and citrate synthase activities and th

126 Any increase in CK-MB levels was associated with poorer clinical outcome

127 myocardial injury as determined by a rise in CK-MB levels (peak value: 1.6-fold [interquartile range

128 A greater rise in CK-MB levels associated with greater acute and late mort

129 A greater rise in CK-MB levels independently associated with an increased

130 suggesting that B-GATA genes play a role in CK responses.

131 No stellar source has been seen in CK Vul, though a radio continuum source was identified a

132 ggesting that TCP14/15 affect early steps in CK signaling.

133 WUE was significantly higher in PM than in CK for most years of the experiment.

134 Our data indicate that in CK-depleted plants exposed to As(V), transcript levels o

135 The increased CK activity in TCP14/15-overexpressing flowers resulted

136 The selective inhibitor CK-2018571 prevents strong binding to actin and promotes

137 ain or application of two ARP2/3 inhibitors, CK-548 and CK-666, blocks VE-cadherin dynamics and cause

138 3 or 4 aberrations (low-CK and intermediate-CK, respectively) who followed aggressive disease course

139 igh-resolution measurements of intracellular CKs in different plant tissues can therefore provide ins

140 of at least one ISOPENTENYLTRANSFERASE (IPT) CK biosynthetic gene in the stem.

141 s applied here to creatine kinase isoenzyme (CK-MB), a cardiac biomarker in ischemic conditions.

142 asured for PDI interaction with the isolated CK domain and the atomic force microscopy images strongl

143 or activity was with ginsenoside-compound K (CK), containing a monosaccharide (glucose) attached at c

144 nt evidence suggests that complex karyotype (CK) defined by the presence of >=3 chromosomal aberratio

145 sult from upregulation of the protein kinase CK-1 in affected neurons, resulting in postranslational

146 stablished a pivotal role for casein kinase (CK)-2-mediated circadian BMAL1-Ser90 phosphorylation (BM

147 t ATP transfer rate through creatine kinase (CK) (k(f)(CKrest)) would be increased, compensating for

148 has not been confirmed with creatine kinase (CK) assays.

149 r results show that routine creatine kinase (CK) blood values, plasma EVs physical characteristics (i

150 the hypothesis that reduced creatine kinase (CK) capacity and flux is associated with this transition

151 ch to NBS with screening by creatine kinase (CK) levels in dried blood spots followed by mutation det

152 Serum creatine kinase (CK) levels were lower (p = 0.025), and reduced cognitive

153 In addition, serum creatine kinase (CK) levels within the Oxford CMS cohort were retrospecti

154 tly reported variant in the creatine kinase (CK) muscle gene, CKM Glu83Gly (rs11559024) with constitu

155 The creatine kinase (CK) reaction plays a critical role in skeletal muscle fu

156 The creatine kinase (CK) system is thought to play an integral role in mainta

157 n cTnT, cardiac troponin I, creatine kinase (CK), CK-myocardial band levels, and skeletal muscle dama

158 ate dehydrogenase (LDH) and creatine kinase (CK), which cardiac troponins being the main accepted bio

159 Inhibition of creatine kinase (CK), which increases cytosolic ADP, in enzyme-isolated i

160 Myoglobin, creatine-kinase (CK) showed increased levels at the start of MP (medians:

161 rystoyltransferase(NMT)-1 and casein-kinase-(CK)-II-alpha prevented Tat.AG- and HIV-1-CRF02_AG-mediat

162 phosphate (HEP) bonds, and creatine kinases (CK) catalyze the transfer of HEP from adenosine triphosp

163 bonds between the C-terminal cysteine knot (CK) domains of 2 monomers.

164 The C-terminal cystine knot (CK) (CTCK) domain in von Willebrand factor (VWF) mediate

165 ted the quantification of all the well known CK isoprenoid metabolites in four different transgenic A

166 osis, whereas those with mutated CLL lacking CK or TP53abs, as well as CK with +12,+19, show the long

167 eraction seen in the structure of G. lamblia CK in complex with AMP-PNP.

168 examine the structural basis for G. lamblia CK inhibition of disulfiram and its analog, thiram, thei

169 ogether, the studies suggest that G. lamblia CK is an attractive drug target for development of novel

170 titutive creatine phosphokinase (CK) levels, CK variation, and inducibility.

171 d with CK cases with 3 or 4 aberrations (low-CK and intermediate-CK, respectively) who followed aggre

172 M41-CK, a virulent lab-adapted strain of IBV, was egg passag

173 to delineate gene expression in the IBV M41-CK and Beau-R strains at subcodon resolution.

174 Similarly, the mammalian CK counterpart, MYO7A, binds to and impinges on CASPASE-

175 n I or T (cTnI or cTnT), creatine kinase-MB (CK-MB), and myoglobin.

176 retic peptide (BNP), and creatine kinase-MB (CK-MB), and TnI and BNP by CART.

177 red a large elevation of creatine kinase-MB (CK-MB), with identical threshold for both procedures.

178 start of MP (medians: myoglobin: 4377 ng/mL, CK: 1442 U/L), peaking 6 h after perfusate exchange (med

179 te exchange (medians: myoglobin: 9206 ng/mL, CK: 3995 U/L) at timepoint 24.

180 EY POINTS: We report that the small molecule CK-2066260 selectively slows the off-rate of Ca(2)(+) fr

181 r:beta-glucuronidase fusions with the MtCRE1 CK receptor gene and a CK response reporter (TWO COMPONE

182 PM) and conventional covering without mulch (CK).

183 In the obese resting heart, the myocardial CK reaction rate is increased, maintaining ATP delivery

184 ass spectrometry (MS) method for analysis of CK biosynthesis and homeostasis at cellular resolution.

185 d RhIPT5), of CK activation (RhLOG8), and of CK putative transporter RhPUP5 genes and to the repressi

186 been established that multiple components of CK energy metabolism are commonly impaired and that thes

187 ortality according to the various degrees of CK-MB increase after TAVR (p < 0.001).

188 rt on the underlying genetic determinants of CK variation in a population of statin users.

189 l role in mediating the regulatory effect of CK on the transcriptions of CKRC1 and CKRC2 genes in the

190 letal muscle, correlated closely with FSR of CK-M, CA-3, and other proteins of various ontologies in

191 ical associations and the clinical impact of CK in CLL.

192 Given the diagnostic importance of CK in determining muscle damage, we tested the associati

193 the variant has an impact on inducibility of CK by trauma through a previously reported case of a hom

194 ays was indicated, based on the induction of CK metabolic and signaling genes, including the CRE1 rec

195 ary to their typical action as inhibitors of CK signalling, these genes are required for CK-mediated

196 High levels of CK were more frequent in patients with EVD than in those

197 Loss of CK in the arista, border cells or proneural clusters of

198 -distance regulation through modification of CK signaling and altering gene expression.

199 In recent years, a large number of CK inhibitors have been synthesized, and one of them is

200 independently associated with higher peak of CK-MB levels (p < 0.01 for all), which translated into i

201 olated troponin complexes in the presence of CK-2066260 (6 vs. 17 s(-1) under control conditions).

202 ill running, was improved in the presence of CK-2066260.

203 ar collisions, has re-opened the question of CK Vul's status.

204 after 3-6 h of WL exposure) up-regulation of CK synthesis (RhIPT3 and RhIPT5), of CK activation (RhLO

205 tion of CK synthesis (RhIPT3 and RhIPT5), of CK activation (RhLOG8), and of CK putative transporter R

206 and signalling mutants to probe the role of CK in this process.

207 Baseline and SDs of CK were on average 18% (P value=6x10(-)(63)) and 24% (P

208 CRE1)-dependent NF activation of a subset of CK-signaling genes as well as of the CK-regulated Nodula

209 l dominance relies on an increased supply of CK to buds.

210 Total wind-erosion of sediment transport of CK was 18.6 g.m(-2) min(-1), which was 16 and 31 times t

211 This leads to the accumulation of CKs in the node within 6 h and in the bud at 24 h and to

212 s is suppressed solely by the application of CKs.

213 tensely as WL Additionally, up-regulation of CKs by WL promotes xylem flux toward the bud, as evidenc

214 was sufficient to repress expression of one CK receptor (AHK4) and one response regulator (AHP6).

215 .4), serum ALT (36 vs. 46 IU/L; P = 0.4), or CK-18 levels (175 vs. 196 U/L; P = 0.9).

216 ynamic expression or absence of EpCAM and/or CKs in CTCs.

217 the largest value in 0-40 cm soil depth over CK treatment.

218 Accordingly, a p27 mutant (p27(CK-)) devoid of Cdk inhibitory nuclear functions enhance

219 as CD45 negative, EpCAM/pan-cytokeratin (pan-CK) double-positive population after excluding debris, d

220 erentially (available in 49.5% of patients), CK-MB otherwise.

221 4) with constitutive creatine phosphokinase (CK) levels, CK variation, and inducibility.

222 In plants, CKs act at trace, often low femtomolar concentrations; t

223 FSR of plasma CK-M and CA-3 revealed changes and interindividual diffe

224 synthesis, and the accumulation of plastidic CKs in pgi1-2 leaves.

225 ts involvement in the synthesis of plastidic CKs in roots.

226 cancer, isolated via CellSearch (EpCAM(pos)/CK(pos)/CD45(neg)/DAPI(pos)) and subsequent FACS sorting

227 d further optimization of a number of potent CK-1delta inhibitors.

228 P14/15 activities and how these TCPs promote CK responses.

229 functionally with TCP14 and TCP15 to promote CK responses.

230 nopathies include myopathic features, raised CK levels and variable mild cognitive delay.

231 How the bps signal down-regulates CK remains unknown, though the bps signal was sufficient

232 and, instead, the bps signal down-regulates CK responses.

233 sal Definition of MI, both of which required CK-MB elevation and electrocardiographic evidence of per

234 c resonance spectroscopy measures of resting CK flux suggest that ATP delivery is reduced earlier, at

235 CVR2B/Fc treatment caused increases in serum CK levels in some Dysf(-/-) mice, indicating possible mu

236 ted a genome-wide association study of serum CK levels in 3412 statin users.

237 So, CK-MB determination has been achieved in mediator free-c

238 nately recognized as plant-based substances, CKs have been found across different domains of life, in

239 As such, targeting CK capacity and flux may be a therapeutic strategy to pr

240 at bud outgrowth is promoted by CK, and that CK synthesis is inhibited by auxin, leading to the hypot

241 We conclude that CK Vul is best explained as the remnant of a merger of t

242 We found that CK signaling mutants and transgenic plants with reduced

243 ed for a given Ca(2+) , we hypothesized that CK-2066260 could mitigate muscle fatigue by reducing the

244 Our data indicate that CK acts as substrate adaptor, recruiting SHAGGY46/GSK3-b

245 Our findings indicate that CK is an important regulatory factor in plant adaptation

246 Here we report that CK Vul is surrounded by chemically rich molecular gas in

247 has peculiar isotopic ratios, revealing that CK Vul's composition was strongly enhanced by the nuclea

248 ructure of the SMM/drug complex reveals that CK-2018571 binds to a novel allosteric pocket that opens

249 Instead, our data suggest that CK acts to overcome auxin-mediated bud inhibition, allow

250 Altogether, these results suggest that CKs are initial components of the light signaling pathwa

251 ing early stages of neurodegeneration in the CK-p25 mouse.

252 4 intra-chain disulfides, including 3 in the CK.

253 Further studies measuring the CK flux in BD are required to confirm and extend this fi

254 er RhPUP5 genes and to the repression of the CK degradation RhCKX1 gene in the node.

255 mulated proteins promote the activity of the CK phosphorelay cascade in developing Arabidopsis leaves

256 treatment and 10.6% lower than those of the CK treatment.

257 overexpression enhanced the response of the CK-induced synthetic promoter pTCS to CK, suggesting tha

258 cognate proteins to profile the brain of the CK-p25-inducible mouse model of Alzheimer's disease-like

259 bset of CK-signaling genes as well as of the CK-regulated Nodulation Signaling Pathway2 and Ethylene

260 that transcript abundance of a clade of the CK-responsive type-A Arabidopsis response regulator (ARR

261 indicate that PDIA1 binds exclusively to the CK domain, suggesting a key role of PDIA1 in VWF dimeriz

262 xpressing differently (DEGs) compared to the CK, respectively.

263 O(2) and warming plus eCO(2) compared to the CK, respectively.

264 Therefore, CK may play both positive and negative roles in M. trunc

265 ONELY GUY3 (LOG3) and LOG4 [8, 9] Therefore, CK was hypothesized to act as a mobile signal from the x

266 ighlights myocardial energy delivery through CK as a potential therapeutic target to improve symptoms

267 onobese heart increases ATP delivery through CK, the obese heart does not; this is associated with re

268 ed failure to replenish ATP from PCr through CK enzyme catalysis during tissue activation.

269 Thus, CK should not be axiomatically considered unfavorable in

270 Exposure to CK-2066260 resulted in a concentration-dependent increas

271 of the CK-induced synthetic promoter pTCS to CK, suggesting that TCP14/15 affect early steps in CK si

272 Total CK capacity is reduced in SevAS, with median values lowe

273 Accompanying the fall in CK flux, total CK and citrate synthase activities and the absolute acti

274 Transgenic CK-deficient Arabidopsis and tobacco lines show a marked

275 he absolute activities of mitochondrial-type CK and CK-MM isoforms were also lower (P<0.02, all analy

276 es were indicative of additional zeatin-type CKs in decapitated stems being supplied by roots and thu

277 rate (FSR) of plasma creatine kinase M-type (CK-M) and carbonic anhydrase 3 (CA-3) in the blood, more

278 Unlike CK treatment, the long-term application of fertilizers i

279 Building upon CK, TP53abs, and immunoglobulin heavy variable gene soma

280 howed down-regulated expression in SA versus CK, whereas 14.3% dramatically hypomethylated genes show

281 onstrating that the rate of ATP transfer via CK, measured noninvasively by magnetic resonance spectro

282 with fluorescence microscopy studies of VWF CK-domain mutants, we suggest the following mechanism of

283 Is defined by isolated enzyme elevation when CK-MB was more than 10 times ULN.

284 levels were normal in all patients, whereas CK-myocardial band levels were increased in 59% of patie

285 While CKs are predominately recognized as plant-based substanc

286 phosphocreatine/ATP (by 17%, P<0.001), with CK k(f) unchanged (P=0.46).

287 nstitutive CK levels is also associated with CK variability and inducibility.

288 was significantly higher in PM compared with CK.

289 Thus, they contrasted with CK cases with 3 or 4 aberrations (low-CK and intermediat

290 cTnT levels correlated with CK levels in all 3 subgroups (P<0.001).

291 Rodents dosed with CK-2066260 show increased hindlimb muscle force and powe

292 Rats dosed with CK-2066260 showed increased hindlimb isometric and isoki

293 orces (i.e. lower stimulation frequency with CK-2066260): force was decreased by ~50% with and by ~75

294 linked intellectual disability in males with CK syndrome.

295 the other end of the spectrum, patients with CK and +12,+19 displayed an exceptionally indolent profi

296 ARTS was used to study the relationship with CK variability.

297 fibres and rat muscles in-situ treated with CK-2066260 showed improved muscle endurance., which was

298 ere diffusion distances correlated well with CK total activity (r=0.86, P=0.003).

299 was increased by ~10% with and ~32% without CK-2066260, reflecting a larger decrease in [ATP] in the

300 s decreased by ~50% with and by ~75% without CK-2066260; [Mg(2+) ](i) was increased by ~10% with and

301 was about two times higher with than without CK-2066260.