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 greatly increased k(tr) at submaximal activat

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

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

9 CK-2066260 shifted the tension-calcium relationship left

10 CK-induced gene expression is partially compromised in L

11 CK-M overexpression significantly increased ATP flux thr

12 CKs 5/6 and 14 were detected in the basal and suprabasal

13 CKs in each monomer flank the 3 inter-chain disulfides,

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

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

16 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

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

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

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

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

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

22 the fast skeletal muscle troponin activator, CK-2066260, on calcium-induced force development was stu

23 tension-pCa relations with and without added CK-2066260.

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

25 molecular weights of PEG, CK(30)PEG(10k) and CK(30)PEG(5k).

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

27 e observed in two animal models, 3xTg-AD and CK-p25.

28 ndent, suggesting a model in which auxin and CK are dominant regulators of decapitation-induced branc

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

30 ss ROR1 reduced expression of E-cadherin and CK-19, but enhanced the expression of SNAIL-1/2 and vime

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

32 Levels of albumin, creatinine, and CK-MB did not show significant changes after LA.

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

34 mmonly have persistent elevation of cTnT and CK-MB in the absence of clinical and cTnI evidence of my

35 mug/l), CK (582 U/l; 303 to 3,662 U/l), and CK-MB (24 mug/l; 8 to 34 mug/l).

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

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

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

39 tissue and time specificity to the aromatic CK 6-benzylaminopurine (BAP) and that fast posttranscrip

40 l as to explore the possibility that the ATM/CK cluster and Ser-271 synergistically or antagonistical

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

42 The ATM/CK cluster phosphorylation attenuates CBP binding and CR

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

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

45 rved phosphorylation cluster, termed the ATM/CK cluster, which is processively phosphorylated in resp

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

47 increasing creatine kinase-myocardial band (CK-MB) thresholds with spontaneous MI.

48 inase (CK), creatine kinase myocardial band (CK-MB), and N-terminal pro-B-type natriuretic peptide (N

49 ncidence of creatine kinase-myocardial band (CK-MB)-defined PPMI (CK-MB >3x upper limit of normal) wa

50 d to replicate the association with baseline CK measures.

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

52 ted a new series of asymmetrical biscationic CK inhibitors by means of enzymatic, crystallographic, a

53 mg/dl was significantly associated with both CK-MB-defined (p = 0.026) and troponin I/T-defined PPMI

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

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

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

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

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

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

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

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

62 ntracellular trafficking of highly compacted CK(30)PEG DNPs made using two different molecular weight

63 (HR, 1.41; P < .001), karyotype complexity (CK [three abnormalities]: HR, 1.81; P = .003; very CK [>

64 R, 1.12; P < .001) and karyotype complexity (CK: HR, 2.53; P = .002; very CK: HR, 2.77; P < .001).

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

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

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

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

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

70 A combination of smoking tobacco, UWS CRP, CK-MB, sCD40 ligand, gender, and number of teeth identif

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

72 orphology and expressing CD133, cytokeratin (CK)7, CK19, procollagen-alpha1(I), and Snail at day 5 af

73 fferentiation-specific markers, cytokeratin (CK) 5/6, 13, and 14, to detect presence or absence of ke

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

75 STM activates cytokinin (CK) biosynthesis in the SAM, but the extent to which STM

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

77 Strigolactone (SL), auxin, and cytokinin (CK) are hormones that interact to regulate shoot branchi

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

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

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

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

82 ibberellin signaling and promotes cytokinin (CK) responses by unknown mechanisms.

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

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

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

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

87 The plant hormones cytokinins (CKs) regulate multiple developmental and physiological p

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

89 light signaling pathway involve cytokinins (CKs).

90 Cytosolic CKs are expressed in a HIF-2-dependent manner in vitro a

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

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

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

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

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

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

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

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

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

100 s post-DEN injection, all LKO mice developed CK-19-positive hepatobiliary cysts, which correlated wit

101 ts in 27 ambulatory patients showed elevated CK (953 U/l; 562 to 1,320 U/l), CK-MB (18 mug/l; 11 to 2

102 by mutation detection in those with elevated CK.

103 procedures did not greatly alter endogenous CK levels.

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

105 xpression phenotypes, including the enhanced CK responses.

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

107 microm) and found that in the NEB KO fibers, CK-2066260 had a larger effect on calcium sensitivity at

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

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

110 e family and have differing requirements for CK and CYCD3.

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

112 f E-cadherin, epithelial cytokeratins (e.g., CK-19), and tight junction proteins (e.g., ZO-1), and im

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

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

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

116 rin, high molecular weight cytokeratins (Hmw CK) and CK5, vimentin) and lineage differentiation (ss-t

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

118 mum two different kinases, casein kinase II (CK II) and tousled-like kinase (tlk).

119 We further conclude that rapid changes in CK status in stems are auxin dependent but largely SL in

120 This difference in CK content may explain why rms buds on explants respond

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

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

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

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

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

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

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

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

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

130 gulation of CK biosynthesis genes, increased CK levels, and down-regulation of auxin transport genes.

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

132 we redefined procedural MI using increasing CK-MB thresholds and compared corresponding hazard ratio

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

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

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

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

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

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

139 tation, ginsenoside Rg1, Rd, and compound K (CK) significantly increased, especially Rd, while other

140 Complex karyotype (CK) is the poorest risk factor in patients with myelodys

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

142 Carbamate kinase (CK) catalyzes the last step in this pathway, converting

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

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

145 Creatine kinase (CK) is a commonly used biomarker to assist in the diagno

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

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

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

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

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

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

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

153 ements of serum cTnT, cTnI, creatine kinase (CK), creatine kinase myocardial band (CK-MB), and N-term

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

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

156 ngiectasia-mutated (ATM) and casein kinases (CKs) 1 and 2.

157 e present study identifies creatine kinases (CKs), key metabolic enzymes for rapid ATP generation via

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

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

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

161 l; interquartile range: 0.06 to 0.14 mug/l), CK (582 U/l; 303 to 3,662 U/l), and CK-MB (24 mug/l; 8 t

162 wed elevated CK (953 U/l; 562 to 1,320 U/l), CK-MB (18 mug/l; 11 to 28 mug/l), and cTnT (0.03 mug/l;

163 ermined two crystal structures of G. lamblia CK (glCK) with bound ligands.

164 reat chronic alcoholism, inhibits G. lamblia CK and kills G. lamblia trophozoites in vitro at submicr

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

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

167 nidazole-resistant strain and the G. lamblia CK irreversible inactivation mechanism show that the thi

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

169 The crystal structure of G. lamblia CK soaked with disulfiram revealed that the compound thi

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

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

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

173 hazard ratios with those of spontaneous MI (CK-MB more than twice the ULN).

174 .0 (i.e., calcium concentrations <1 microM), CK-2066260 increased tension of NEB KO fibers to beyond

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

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

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

178 al between serum levels of CK and the muscle CK (CKM) gene (rs11559024: P=3.69x10(-16); R(2)=0.02) an

179 tibialis cranialis fibers in the absence of CK-2066260 was approximately 60% less than in WT fibers,

180 BP, but not KNAT2, despite its activation of CK responses, suggesting that promotion of CK responses

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

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

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

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

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

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

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

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

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

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

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

192 g association signal between serum levels of CK and the muscle CK (CKM) gene (rs11559024: P=3.69x10(-

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

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

195 into hepatic lineage by progressive loss of CK-19/laminin expression and appearance of C/EBP-alpha e

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

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

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

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

200 f CK responses, suggesting that promotion of CK responses alone is insufficient for SAM organisation.

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

202 -induced myotoxicity but the normal range of CK concentrations is wide, which limits its use as a dia

203 xplants both showed similar up-regulation of CK biosynthesis genes, increased CK levels, and down-reg

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 he basal and suprabasal layers, and spots of CK 13 were detected in the suprabasal layer.

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

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

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 Involvement of CKs in PS phosphorylation was confirmed using purified C

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

215 However, the tissue-specific targets of CKs and the mechanisms underlying such specificity remai

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

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

218 opically, even when CK levels are reduced or CK signaling is impaired.

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

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

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

222 via the phosphocreatine-creatine kinase (PCr/CK) system, as a unique gene family that is coordinately

223 Further, enzymes of the PCr/CK metabolic shuttle demonstrate dysregulated mucosal ex

224 sing two different molecular weights of PEG, CK(30)PEG(10k) and CK(30)PEG(5k).

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

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

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

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

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

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

231 kinase-myocardial band (CK-MB)-defined PPMI (CK-MB >3x upper limit of normal) was 5.8% and associated

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

233 functionally with TCP14 and TCP15 to promote CK responses.

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

235 findings establish a role for HIF-regulated CK in epithelial homeostasis and reveal a fundamental li

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

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

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

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

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

241 Consequently, brain penetrant specific CK-1 inhibitors may provide a new therapeutic strategy f

242 ficance of which is less well validated than CK-MB.

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

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

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

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

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

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

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

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

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

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

253 endoreduplication, acting through CK and the CK-inducible CYCD3 cell cycle regulators, establishing a

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

255 4 intra-chain disulfides, including 3 in the CK.

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

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

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

259 cant differences between the kinetics of the CK reaction among muscle groups.

260 P-MRI method for mapping the kinetics of the CK reaction, and the unidirectional phosphocreatine (PCr

261 the sarcomere length (SL) dependence of the CK-2066260 effect (SL 2.1 microm and 2.6 microm) and fou

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

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

264 responses, as well as the expression of the CK-regulated gene RESPONSE REGULATOR5.

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

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

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

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

269 iation and endoreduplication, acting through CK and the CK-inducible CYCD3 cell cycle regulators, est

270 ion significantly increased ATP flux through CK ex vivo and in vivo but did not alter contractile fun

271 nt to which STM function is mediated through CK is unclear.

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

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

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

275 ent organs and tissues (e.g. the response to CKs has been shown to be opposite in shoot and root samp

276 Responses to CKs vary in different organs and tissues (e.g. the respo

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

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

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

280 SPY-dependent manner and stimulated typical CK morphological responses, as well as the expression of

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

282 ype complexity (CK: HR, 2.53; P = .002; very CK: HR, 2.77; P < .001).

283 ree abnormalities]: HR, 1.81; P = .003; very CK [> three abnormalities]: HR, 2; P < .001), and abnorm

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

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

286 mation when expressed ectopically, even when CK levels are reduced or CK signaling is impaired.

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

288 e 2 genes were independently associated with CK levels in statin users.

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

290 was significantly higher in PM compared with CK.

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

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

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

294 linked intellectual disability in males with CK syndrome.

295 Blocking actin nucleation with CK-666, a specific inhibitor of the Arp2/3 complex, prot

296 (MK) worsens the prognosis of patients with CK.

297 nts (16%), most of whom (88%) presented with CK.

298 rial sections, oval cell proliferations with CK-19(+)/laminin(+) and OV-6(+)/C/EBP-alpha(-) were show

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

300 Importantly, treatment with CK-666 attenuated a decrease in occludin levels in brain

301 um sativum) have SL defects, perturbed xylem CK levels, and diminished responses to auxin in shoot de