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Creatine kinase, muscle

muscle creatine kinase, MCK, CKM, CKMM
The protein encoded by this gene is a cytoplasmic enzyme involved in energy homeostasis and is an important serum marker for myocardial infarction. The encoded protein reversibly catalyzes the transfer of phosphate between ATP and various phosphogens such as creatine phosphate. It acts as a homodimer in striated muscle as well as in other tissues, and as a heterodimer with a similar brain isozyme in heart. The encoded protein is a member of the ATP:guanido phosphotransferase protein family. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, ACID, MyoD, Myogenin
Papers using muscle creatine kinase antibodies
SHP-2 activates signaling of the nuclear factor of activated T cells to promote skeletal muscle growth
Bennett Anton M. et al., In The Journal of Cell Biology, 2003
... floxed allele was generated in a 129Sv/B6 mixed background, crossed with MCK-Cre transgenic mice to obtain SHP-2 ...
Viral vectors for gene transfer of micro-, mini-, or full-length dystrophin
Kim Jason K. et al., In Diabetes, 2001
... E-box sites and a proximal regulatory region of the muscle creatine kinase gene differentially regulate expression in diverse skeletal muscles and cardiac muscle of transgenic mice ...
Expression of α7 integrin cytoplasmic domains during skeletal muscle development: Alternate forms, conformational change, and homologies with serine/threonine kinases and tyrosine phosphatases.
Phillips Stuart M., In PLoS ONE, 1992
... α7Tg mice (MCK- α7BX2) were produced at the University of Illinois Transgenic Animal Facility as described ...
Papers on muscle creatine kinase
Evaluation of the Relative Performance of Drug-Induced Skeletal Muscle Injury Biomarkers in Rats.
Glaab et al., Central African Republic. In Toxicol Sci, Jan 2016
The relative performance of these novel biomarkers of SKM injury including skeletal troponin I (sTnI), myosin light chain 3 (Myl3), creatine kinase M Isoform (Ckm), and fatty acid binding protein 3 (Fabp3) was assessed in 34 rat studies including both SKM toxicants and compounds with toxicities in tissues other than SKM.
The Mediator Kinase Module Restrains Epidermal Growth Factor Receptor Signaling and Represses Vulval Cell Fate Specification in Caenorhabditis elegans.
Taubert et al., Colombia. In Genetics, Jan 2016
Here, we show that Mediator's dissociable Cyclin Dependent Kinase 8 (CDK8) Module (CKM), consisting of cdk-8, cic-1/Cyclin C, mdt-12/dpy-22, and mdt-13/let-19, is required to inhibit ectopic vulval cell fates downstream of the epidermal growth factor receptor (EGFR)-Ras-extracellular signal-regulated kinase (ERK) pathway.
Retinol as a cofactor for PKCδ-mediated impairment of insulin sensitivity in a mouse model of diet-induced obesity.
Hammerling et al., New York City, United States. In Faseb J, Jan 2016
We crossed mice overexpressing human retinol-binding protein (hRBP) under the muscle creatine kinase (MCK) promoter (MCKhRBP) with the PKCδ(-/-) strain to generate mice with a different status of the PKCδ signalosome and retinoid levels.
Resistance to thyroid hormone due to defective thyroid receptor alpha.
Chatterjee et al., Cambridge, United Kingdom. In Best Pract Res Clin Endocrinol Metab, Aug 2015
Biochemical abnormalities include low/low-normal T4 and high/high-normal T3 concentrations, a subnormal T4/T3 ratio, variably reduced reverse T3, raised muscle creatine kinase and mild anaemia.
Association of Plasma Heat Shock Protein 70, Interleukin 6, and Creatine Kinase Concentrations in a Healthy, Young Adult Population.
Deuster et al., Bethesda, United States. In J Biomark, 2014
Mean protein levels of CK, HSP70, and IL-6 were compared by sex, ethnicity, genetic variants-CKMM Nco1 (rs1803285), HSPA1B +A1538G (rs1061581), and IL6 G-174C (rs1800795)-self-reported history of exercise, oral contraceptive use, and dietary supplement use.
Activated Integrin-Linked Kinase Negatively Regulates Muscle Cell Enhancement Factor 2C in C2C12 Cells.
Cang et al., Hohhot, China. In Biomed Res Int, 2014
We inhibited PI3K activity in C2C12 with LY294002 and then found that ILK phosphorylation levels and MEF2C phosphorylation were decreased and that MCK mRNA expression was suppressed significantly.
Prevention and reversal of severe mitochondrial cardiomyopathy by gene therapy in a mouse model of Friedreich's ataxia.
Puccio et al., Illkirch-Graffenstaden, France. In Nat Med, 2014
A conditional mouse model with complete frataxin deletion in cardiac and skeletal muscle (Mck-Cre-Fxn(L3/L-) mice) recapitulates most features of FRDA cardiomyopathy, albeit with a more rapid and severe course.
Skeletal muscle hypertrophy and regeneration: interplay between the myogenic regulatory factors (MRFs) and insulin-like growth factors (IGFs) pathways.
Gailly et al., Brussels, Belgium. In Cell Mol Life Sci, 2013
The MRF family of proteins controls the transcription of important muscle-specific proteins such as myosin heavy chain and muscle creatine kinase.
Regulation of sodium-calcium exchanger activity by creatine kinase.
Kao et al., Taipei, Taiwan. In Adv Exp Med Biol, 2012
Among the four creatine kinase (CK) isozymes, both sMiCK and the muscle-type cytosolic creatine kinase (CKM) co-immunoprecipitated with NCX1.
Creatine kinase MM TaqI and methylenetetrahydrofolate reductase C677T and A1298C gene polymorphisms influence exercise-induced C-reactive protein levels.
Klautau-Guimarães et al., Brasília, Brazil. In Eur J Appl Physiol, 2012
Creatine kinase MM TaqI and methylenetetrahydrofolate reductase C677T and A1298C gene polymorphisms influence exercise-induced C-reactive protein levels.
Creatine kinase MM TaqI and methylenetetrahydrofolate reductase C677T and A1298C gene polymorphisms influence exercise-induced C-reactive protein levels.
Klautau-Guimarães et al., Brasília, Brazil. In Eur J Appl Physiol, 2012
Results indicate that these polymorphisms can indirectly influence performance, contribute to higher susceptibility to exercise-induced inflammation or protection against it, and perhaps affect future risks of CVD in athletes.
Creatine kinase-mediated improvement of function in failing mouse hearts provides causal evidence the failing heart is energy starved.
Weiss et al., Baltimore, United States. In J Clin Invest, 2012
CK-M overexpression led to significantly increased contractile function at baseline and during adrenergic stimulation and increased survival after thoracic aortic constriction-induced heart failure.
Muscle creatine kinase deficiency triggers both actin depolymerization and desmin disorganization by advanced glycation end products in dilated cardiomyopathy.
Mericskay et al., Paris, France. In J Biol Chem, 2011
strong down-regulation of MCK activity contributes to F-actin instability and induces post-translational modification of alphaB-crystallin and desmin
Dissimilarity in the folding of human cytosolic creatine kinase isoenzymes.
Yan et al., Beijing, China. In Plos One, 2010
The results suggested that the intra- and inter-subunit domain interactions modified the behavior of kinetic refolding.
Model mice for tissue-specific deletion of the manganese superoxide dismutase gene.
Shirasawa et al., Tokyo, Japan. In Geriatr Gerontol Int, 2010
Next, we generated heart/muscle-specific Mn-SOD-deficient mice by crossbreeding muscle creatine kinase-Cre transgenic mice.
Nfix regulates fetal-specific transcription in developing skeletal muscle.
Cossu et al., Milano, Italy. In Cell, 2010
We show here that the transcription factor nuclear factor one X (Nfix), whose expression is activated by Pax7 in fetal muscle, in turn activates the transcription of fetal specific genes such as MCK and beta-enolase while repressing embryonic genes such as slow myosin.
A potential link between muscle peroxisome proliferator- activated receptor-alpha signaling and obesity-related diabetes.
Kelly et al., Saint Louis, United States. In Cell Metab, 2005
Transgenic mice overexpressing PPARalpha in muscle (MCK-PPARalpha mice) developed glucose intolerance despite being protected from diet-induced obesity.
Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres.
Spiegelman et al., Boston, United States. In Nature, 2002
When PGC-1 alpha is expressed at physiological levels in transgenic mice driven by a muscle creatine kinase (MCK) promoter, a fibre type conversion is observed: muscles normally rich in type II fibres are redder and activate genes of mitochondrial oxidative metabolism.
Monaco et al., Seattle, United States. In Unknown Journal, 2002
Increased serum concentration of muscle creatine kinase (CK) is observed in the majority of affected individuals.
Skeletal muscles of mice deficient in muscle creatine kinase lack burst activity.
Wieringa et al., Nijmegen, Netherlands. In Cell, 1993
To understand the physiological role of the creatine kinase-phosphocreatine (CK-PCr) system in muscle bioenergetics, a null mutation of the muscle CK (M-CK) gene was introduced into the germline of mice.
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