Gene Symbol: Ckm
Description: creatine kinase, muscle
Alias: CPK-M, Ckmm, M-CK, MCK, creatine kinase M-type, creatine kinase M chain, creatine phosphokinase M-type
Species: mouse
Products:     Ckm

Top Publications

  1. Kaasik A, Veksler V, Boehm E, Novotova M, Ventura Clapier R. From energy store to energy flux: a study in creatine kinase-deficient fast skeletal muscle. FASEB J. 2003;17:708-10 pubmed
    ..These results demonstrate two possible patterns of energy transport in muscle cells: energy store with phosphocreatine and energy flux through mitochondria. ..
  2. Buskin J, Jaynes J, Chamberlain J, Hauschka S. The mouse muscle creatine kinase cDNA and deduced amino acid sequences: comparison to evolutionarily related enzymes. J Mol Evol. 1985;22:334-41 pubmed
  3. Roman B, Wieringa B, Koretsky A. Functional equivalence of creatine kinase isoforms in mouse skeletal muscle. J Biol Chem. 1997;272:17790-4 pubmed
    ..These results indicate that CK compartmentation to the myofibril of skeletal muscle is not essential for contractile function and that there is functional equivalence of creatine kinase isoforms in supporting cellular energy metabolism. ..
  4. Takahashi C, Contreras B, Bronson R, Loda M, Ewen M. Genetic interaction between Rb and K-ras in the control of differentiation and tumor suppression. Mol Cell Biol. 2004;24:10406-15 pubmed
    ..These observations suggest that Rb and K-ras function together in vivo, in the contexts of both embryonic and tumor development, and that the ability to affect differentiation is a major facet of the tumor suppressor function of pRb. ..
  5. Seale P, Bjork B, Yang W, Kajimura S, Chin S, Kuang S, et al. PRDM16 controls a brown fat/skeletal muscle switch. Nature. 2008;454:961-7 pubmed publisher
    ..Taken together, these data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myoblast markers and is not involved in white adipogenesis. ..
  6. Roman B, Meyer R, Wiseman R. Phosphocreatine kinetics at the onset of contractions in skeletal muscle of MM creatine kinase knockout mice. Am J Physiol Cell Physiol. 2002;283:C1776-83 pubmed
    ..Taken together, the results suggest that cytoplasmic ADP more rapidly increases and oxidative phosphorylation is more rapidly activated at the onset of contractions in MMKO compared with WT muscles. ..
  7. Lluis F, Ballestar E, Suelves M, Esteller M, Munoz Canoves P. E47 phosphorylation by p38 MAPK promotes MyoD/E47 association and muscle-specific gene transcription. EMBO J. 2005;24:974-84 pubmed
    ..These findings identify a novel pro-myogenic role of p38 in regulating the formation of functional MyoD/E47 heterodimers that are essential for myogenesis. ..
  8. Shanti K, Kanungo M. Expression of muscle creatine kinase gene of mice and interaction of nuclear proteins with MEF-2, E boxes and A/T-rich elements during aging. Mol Biol Rep. 2004;31:43-50 pubmed
    The changes in the expression of muscle creatine kinase (MCK) gene in the heart and skeletal muscle of mice during aging were studied...
  9. Shannon M, Ashworth L, Mucenski M, Lamerdin J, Branscomb E, Stubbs L. Comparative analysis of a conserved zinc finger gene cluster on human chromosome 19q and mouse chromosome 7. Genomics. 1996;33:112-20 pubmed
    ..These studies pave the way for a systematic analysis of the evolution of structure and function of genes within the numerous clustered ZNF families located on human chromosome 19 and elsewhere in the human and mouse genomes. ..

More Information


  1. Filali M, Lalonde R, Gérard C, Coulombe Z, Tremblay J. Sensorimotor skills in Fxn KO/Mck mutants deficient for frataxin in muscle. Brain Res. 2015;1608:91-6 pubmed publisher
    ..The Fxn KO/Mck model reproduces some key features of patients with Friedreich ataxia and provides an opportunity of ameliorating ..
  2. Veksler V, Kuznetsov A, Anflous K, Mateo P, van Deursen J, Wieringa B, et al. Muscle creatine kinase-deficient mice. II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the mitochondrial function. J Biol Chem. 1995;270:19921-9 pubmed
  3. Koyama S, Hata S, Witt C, Ono Y, Lerche S, Ojima K, et al. Muscle RING-finger protein-1 (MuRF1) as a connector of muscle energy metabolism and protein synthesis. J Mol Biol. 2008;376:1224-36 pubmed publisher
  4. Hasty P, Bradley A, Morris J, Edmondson D, Venuti J, Olson E, et al. Muscle deficiency and neonatal death in mice with a targeted mutation in the myogenin gene. Nature. 1993;364:501-6 pubmed
    ..Myogenin-mutant mice differ from mice carrying mutations in genes for the related myogenic factors Myf5 and MyoD, which have no muscle defects. Myogenin is therefore essential for the development of functional skeletal muscle. ..
  5. Steeghs K, Benders A, Oerlemans F, de Haan A, Heerschap A, Ruitenbeek W, et al. Altered Ca2+ responses in muscles with combined mitochondrial and cytosolic creatine kinase deficiencies. Cell. 1997;89:93-103 pubmed
    ..Our data point to a direct link between the CK-PCr system and Ca2+-flux regulation during the excitation and relaxation phases of muscle contraction. ..
  6. Araya R, Eckardt D, Maxeiner S, Krüger O, Theis M, Willecke K, et al. Expression of connexins during differentiation and regeneration of skeletal muscle: functional relevance of connexin43. J Cell Sci. 2005;118:27-37 pubmed
    ..Thus, the expression of Cx45 and Cx43 is upregulated during skeletal muscle regeneration and Cx43 is required for normal myogenesis in vitro and adult muscle regeneration in vivo. ..
  7. Nuss J, Amaning J, Bailey C, DeFord J, Dimayuga V, Rabek J, et al. Oxidative modification and aggregation of creatine kinase from aged mouse skeletal muscle. Aging (Albany NY). 2009;1:557-72 pubmed
    ..Muscle creatine kinase (CKm) activity maintains energetic homeostasis as variations in energy requirements dictate that ATP be readily ..
  8. Dahlstedt A, Katz A, Westerblad H. Role of myoplasmic phosphate in contractile function of skeletal muscle: studies on creatine kinase-deficient mice. J Physiol. 2001;533:379-88 pubmed
    ..Increased P(i) appears to be involved in both fatigue-induced changes of cross-bridge function and SR Ca(2+) handling. ..
  9. de Groof A, Smeets B, Groot Koerkamp M, Mul A, Janssen E, Tabak H, et al. Changes in mRNA expression profile underlie phenotypic adaptations in creatine kinase-deficient muscles. FEBS Lett. 2001;506:73-8 pubmed
    ..Our results reveal that regulation of transcript level plays an important role, but it is not the only principle involved in the remodeling of mitochondrial and cytosolic design of CK(-/-) muscles. ..
  10. Gorselink M, Drost M, Van der Vusse G. Murine muscles deficient in creatine kinase tolerate repeated series of high-intensity contractions. Pflugers Arch. 2001;443:274-9 pubmed
    ..These findings indicate that CK-/- tolerate repeated series of high-intensity contractions better than WT, while in CK-/- muscle an additional source of energy is mobilised to regenerate ATP during the second series. ..
  11. Dahlstedt A, Katz A, Wieringa B, Westerblad H. Is creatine kinase responsible for fatigue? Studies of isolated skeletal muscle deficient in creatine kinase. FASEB J. 2000;14:982-90 pubmed
    ..However, during more prolonged stimulation, CK may contribute to the fatigue process by increasing the myoplasmic concentration of inorganic phosphate. ..
  12. Fowlis G, Fairchild S, Tomonari K, Simpson E. Toward identification of minor histocompatibility antigens in mouse and man. Transplant Proc. 1992;24:1689-91 pubmed
  13. Nagandla H, Lopez S, Yu W, Rasmussen T, Tucker H, Schwartz R, et al. Defective myogenesis in the absence of the muscle-specific lysine methyltransferase SMYD1. Dev Biol. 2016;410:86-97 pubmed publisher
    ..Thus, in addition to the previously described functions for Smyd1 in heart development and skeletal muscle sarcomerogenesis, these results point to a novel role for Smyd1 in myoblast differentiation. ..
  14. Gupta A, Akki A, Wang Y, Leppo M, Chacko V, Foster D, et al. Creatine kinase-mediated improvement of function in failing mouse hearts provides causal evidence the failing heart is energy starved. J Clin Invest. 2012;122:291-302 pubmed publisher
    ..In addition, these data identify CK as a promising therapeutic target for preventing and treating HF and possibly diseases involving energy-dependent dysfunction in other organs with temporally varying energy demands. ..
  15. Gorselink M, Drost M, Coumans W, van Kranenburg G, Hesselink R, Van der Vusse G. Impaired muscular contractile performance and adenine nucleotide handling in creatine kinase-deficient mice. Am J Physiol Endocrinol Metab. 2001;281:E619-25 pubmed
    ..ATP regeneration via the adenylate kinase pathway is a likely cause of reduced basal adenine nucleotide levels in CK(-/-) mice...
  16. Watchko J, Daood M, Sieck G, Labella J, Ameredes B, Koretsky A, et al. Combined myofibrillar and mitochondrial creatine kinase deficiency impairs mouse diaphragm isotonic function. J Appl Physiol (1985). 1997;82:1416-23 pubmed
    ..We conclude that combined myofibrillar and sarcomeric mitochondrial CK deficiency profoundly impairs Dia power and work output, underscoring the functional importance of CK during dynamic contractions in skeletal muscle...
  17. Liu Z, Li W, Ma X, Ding N, Spallotta F, Southon E, et al. Essential role of the zinc finger transcription factor Casz1 for mammalian cardiac morphogenesis and development. J Biol Chem. 2014;289:29801-16 pubmed publisher
    ..that are critical for muscular system development and function, such as muscle contraction genes TNNI2, TNNT1, and CKM; contractile fiber gene ACTA1; and cardiac arrhythmia associated ion channel coding genes ABCC9 and CACNA1D...
  18. Nitzki F, Zibat A, Frommhold A, Schneider A, Schulz Schaeffer W, Braun T, et al. Uncommitted precursor cells might contribute to increased incidence of embryonal rhabdomyosarcoma in heterozygous Patched1-mutant mice. Oncogene. 2011;30:4428-36 pubmed publisher
  19. Vivian J, Gan L, Olson E, Klein W. A hypomorphic myogenin allele reveals distinct myogenin expression levels required for viability, skeletal muscle development, and sternum formation. Dev Biol. 1999;208:44-55 pubmed
  20. Jaleel M, Nichols R, Deak M, Campbell D, Gillardon F, Knebel A, et al. LRRK2 phosphorylates moesin at threonine-558: characterization of how Parkinson's disease mutants affect kinase activity. Biochem J. 2007;405:307-17 pubmed
    ..The results of the present study suggest that moesin, ezrin and radixin may be LRRK2 substrates, findings that have been exploited to develop the first robust quantitative assay to measure LRRK2 kinase activity. ..
  21. Jiang Z, Liang P, Leng R, Guo Z, Liu Y, Liu X, et al. E2F1 and p53 are dispensable, whereas p21(Waf1/Cip1) cooperates with Rb to restrict endoreduplication and apoptosis during skeletal myogenesis. Dev Biol. 2000;227:8-41 pubmed
    ..Thus, combined inactivation of Rb and p21(Waf1/Cip1) augments endoreduplication and apoptosis, whereas E2F1 and p53 are dispensable during aberrant myogenesis in Rb-deficient fetuses. ..
  22. Nahrendorf M, Streif J, Hiller K, Hu K, Nordbeck P, Ritter O, et al. Multimodal functional cardiac MRI in creatine kinase-deficient mice reveals subtle abnormalities in myocardial perfusion and mechanics. Am J Physiol Heart Circ Physiol. 2006;290:H2516-21 pubmed
    ..The myocardium in CK-deficient mice is characterized by reduced perfusion and reduced maximal contraction velocity, suggesting that the myocardial hypertrophy seen in these mice cannot fully compensate for the absence of the CK system. ..
  23. Diguet N, Mallat Y, Ladouce R, Clodic G, Prola A, Tritsch E, et al. Muscle creatine kinase deficiency triggers both actin depolymerization and desmin disorganization by advanced glycation end products in dilated cardiomyopathy. J Biol Chem. 2011;286:35007-19 pubmed publisher
    ..We identified muscle creatine kinase (MCK) as the primary down-regulated protein followed by ?-actin and ?-tropomyosin down-regulation leading to a decrease ..
  24. Hagios C, Brown Luedi M, Chiquet Ehrismann R. Tenascin-Y, a component of distinctive connective tissues, supports muscle cell growth. Exp Cell Res. 1999;253:607-17 pubmed
    ..Furthermore, we found that tenascin-Y influenced cell morphology of chick embryo fibroblasts over prolonged times in culture and that it supports primary muscle cell growth and restricts muscle cell differentiation. ..
  25. de Groof A, Oerlemans F, Jost C, Wieringa B. Changes in glycolytic network and mitochondrial design in creatine kinase-deficient muscles. Muscle Nerve. 2001;24:1188-96 pubmed
    ..Adaptations in the network for oxidative adenosine triphosphate (ATP) production are already apparent at 17 days of age. ..
  26. Kernec F, Unlu M, Labeikovsky W, Minden J, Koretsky A. Changes in the mitochondrial proteome from mouse hearts deficient in creatine kinase. Physiol Genomics. 2001;6:117-28 pubmed
    ..We have also detected a large decrease in the precursor form of aconitase. Furthermore, two mitochondrial protein differences have been found in the parent mouse strains of the DbKO-CK mice...
  27. Patapoutian A, Yoon J, Miner J, Wang S, Stark K, Wold B. Disruption of the mouse MRF4 gene identifies multiple waves of myogenesis in the myotome. Development. 1995;121:3347-58 pubmed
    ..Finally, a later and relatively mild phenotype was detected in intercostal muscles of newborn animals. ..
  28. Bulfield G, Siller W, Wight P, Moore K. X chromosome-linked muscular dystrophy (mdx) in the mouse. Proc Natl Acad Sci U S A. 1984;81:1189-92 pubmed
    ..Linkage analysis with four X chromosome loci indicates that mdx maps in the Hq Bpa region of the mouse X chromosome. This gives a gene order of mdx-Tfm-Pgk-1-Ags, the same as for the equivalent genes on the human X chromosome. ..
  29. Saunders A, Seldin M. The syntenic relationship of proximal mouse chromosome 7 and the myotonic dystrophy gene region on human chromosome 19q. Genomics. 1990;6:324-32 pubmed
    ..Their order from the centromere was Prkcg, [Apoe, Atpa-2, Ckmm, D19S19h, Ercc-2], Cyp2b, Mag, Lhb...
  30. van Deursen J, Heerschap A, Oerlemans F, Ruitenbeek W, Jap P, ter Laak H, et al. Skeletal muscles of mice deficient in muscle creatine kinase lack burst activity. Cell. 1993;74:621-31 pubmed
    ..Strikingly, PCr levels decline normally during muscle exercise, suggesting that M-CK-mediated conversion is not the only route for PCr utilization in active muscle. ..
  31. in t Zandt H, de Groof A, Renema W, Oerlemans F, Klomp D, Wieringa B, et al. Presence of (phospho)creatine in developing and adult skeletal muscle of mice without mitochondrial and cytosolic muscle creatine kinase isoforms. J Physiol. 2003;548:847-58 pubmed
  32. Rawls A, Valdez M, Zhang W, Richardson J, Klein W, Olson E. Overlapping functions of the myogenic bHLH genes MRF4 and MyoD revealed in double mutant mice. Development. 1998;125:2349-58 pubmed
  33. Watchko J, Daood M, Wieringa B, Koretsky A. Myofibrillar or mitochondrial creatine kinase deficiency alone does not impair mouse diaphragm isotonic function. J Appl Physiol (1985). 2000;88:973-80 pubmed
    ..We conclude that Dia power and work output are not absolutely dependent on the presence of either M-CK or ScCKmit, whereas the complete absence of CK acutely impairs Dia shortening capacity during repetitive activation...
  34. Washabaugh C, Ontell M, Kant J, Ontell M. Creatine kinase transcript accumulation: effect of nerve during muscle development. Dev Dyn. 1999;215:285-96 pubmed
    ..the lumbosacral spinal cords of 14-day gestation mice (E14) were laser ablated, and the accumulation of muscle CK (MCK) and brain CK (BCK) mRNAs was evaluated just prior to birth with in situ hybridization...
  35. Martin K, Walsh K, Mader S. The mouse creatine kinase paired E-box element confers muscle-specific expression to a heterologous promoter. Gene. 1994;142:275-8 pubmed
    ..the tissue-specific expression properties of the paired murine E-box element from the mouse muscle creatine kinase (MCK) enhancer in a minimal heterologous promoter construct...
  36. Brown S, Chartier F, Johnson K, Cavanna J. Mapping the Hrc gene to proximal mouse chromosome 7: delineation of a conserved linkage group with human 19q. Genomics. 1993;18:459-61 pubmed
  37. Pazin D, Gamer L, Cox K, Rosen V. Molecular profiling of synovial joints: use of microarray analysis to identify factors that direct the development of the knee and elbow. Dev Dyn. 2012;241:1816-26 pubmed publisher
    ..Our microarray analyses provides a new resource for further investigation of the pathways involved in the morphogenesis of specific synovial joints. ..
  38. Gustafson L, van Beek J. Activation time of myocardial oxidative phosphorylation in creatine kinase and adenylate kinase knockout mice. Am J Physiol Heart Circ Physiol. 2002;282:H2259-64 pubmed
  39. Yamane A, Mayo M, Shuler C, Crowe D, Ohnuki Y, Dalrymple K, et al. Expression of myogenic regulatory factors during the development of mouse tongue striated muscle. Arch Oral Biol. 2000;45:71-8 pubmed
  40. Zhang W, Behringer R, Olson E. Inactivation of the myogenic bHLH gene MRF4 results in up-regulation of myogenin and rib anomalies. Genes Dev. 1995;9:1388-99 pubmed
    ..These results demonstrate an unanticipated regulatory relationship between myogenin and MRF4 and suggest that MRF4 influences rib outgrowth through an indirect mechanism. ..
  41. Kan H, Veltien A, Arnts H, Nabuurs C, Luijten B, de Haan A, et al. Gated dynamic 31P MRS shows reduced contractile phosphocreatine breakdown in mice deficient in cytosolic creatine kinase and adenylate kinase. NMR Biomed. 2009;22:523-31 pubmed publisher
  42. Vaarmann A, Fortin D, Veksler V, Momken I, Ventura Clapier R, Garnier A. Mitochondrial biogenesis in fast skeletal muscle of CK deficient mice. Biochim Biophys Acta. 2008;1777:39-47 pubmed
    ..These results evidence that mitochondrial biogenesis in response to a metabolic challenge exhibits a unique pattern of regulation, involving activation of the AMPK pathway. ..
  43. van Deursen J, Wieringa B. Targeting of the creatine kinase M gene in embryonic stem cells using isogenic and nonisogenic vectors. Nucleic Acids Res. 1992;20:3815-20 pubmed
    ..originating from different mouse strains were used to introduce site-specific mutations into the creatine kinase M (CKM) gene of mouse embryonic stem (ES) cells...
  44. Miner J, Miller J, Wold B. Skeletal muscle phenotypes initiated by ectopic MyoD in transgenic mouse heart. Development. 1992;114:853-60 pubmed
  45. He K, Hu J, Yu H, Wang L, Tang F, Gu J, et al. Serine/Threonine Kinase 40 (Stk40) Functions as a Novel Regulator of Skeletal Muscle Differentiation. J Biol Chem. 2017;292:351-360 pubmed publisher
    ..Together, our study reveals that Stk40 is required for fetal skeletal muscle development and provides molecular insights into the control of the HDAC5-MEF2 axis in skeletal myogenesis. ..
  46. Spindler M, Meyer K, Strömer H, Leupold A, Boehm E, Wagner H, et al. Creatine kinase-deficient hearts exhibit increased susceptibility to ischemia-reperfusion injury and impaired calcium homeostasis. Am J Physiol Heart Circ Physiol. 2004;287:H1039-45 pubmed
    ..This demonstrates a key function of an intact CK system for maintenance of Ca2+ homeostasis and LV mechanics under metabolic stress conditions. ..
  47. Janssen E, Terzic A, Wieringa B, Dzeja P. Impaired intracellular energetic communication in muscles from creatine kinase and adenylate kinase (M-CK/AK1) double knock-out mice. J Biol Chem. 2003;278:30441-9 pubmed
    ..Thus, this study suggests a coordinated network of complementary enzymatic pathways that serve in the maintenance of energetic homeostasis and physiological efficiency. ..
  48. Nigro J, Schweinfest C, Rajkovic A, Pavlovic J, Jamal S, Dottin R, et al. cDNA cloning and mapping of the human creatine kinase M gene to 19q13. Am J Hum Genet. 1987;40:115-25 pubmed
    ..Since greater than 69% of the grains of chromosome 19 label band q13, the human creatine kinase-M gene has been mapped to 19q13. On the basis of high-resolution G-banding, the predominant labeling site was 19q13.2-q13.3. ..
  49. Novotova M, Pavlovicová M, Veksler V, Ventura Clapier R, Zahradnik I. Ultrastructural remodeling of fast skeletal muscle fibers induced by invalidation of creatine kinase. Am J Physiol Cell Physiol. 2006;291:C1279-85 pubmed
    ..Using quantitative arguments, we have shown for the first time that spatial relations among organelles of muscle cells undergo adaptation in response to nonstructural stimuli like metabolic deficiency. ..
  50. Fujimoto K, Hamaguchi H, Hashiba T, Nakamura T, Kawamoto T, Sato F, et al. Transcriptional repression by the basic helix-loop-helix protein Dec2: multiple mechanisms through E-box elements. Int J Mol Med. 2007;19:925-32 pubmed
    ..These findings indicate that Dec2 employs multiple mechanisms, including DNA-binding and protein-protein interactions, to achieve E-box-dependent transcriptional repressions. ..
  51. Dong Z, Pan W, Wu H, Liu D, Cang M. Activated Integrin-Linked Kinase Negatively Regulates Muscle Cell Enhancement Factor 2C in C2C12 Cells. Biomed Res Int. 2015;2015:748470 pubmed publisher
    ..with LY294002 and then found that ILK phosphorylation levels and MEF2C phosphorylation were decreased and that MCK mRNA expression was suppressed significantly...
  52. Crozatier B, Badoual T, Boehm E, Ennezat P, Guenoun T, Su J, et al. Role of creatine kinase in cardiac excitation-contraction coupling: studies in creatine kinase-deficient mice. FASEB J. 2002;16:653-60 pubmed
    ..This shows the specific role of CK in excitation-contraction coupling in cardiac muscle that cannot be compensated for by other pathways. ..
  53. Cavanna J, Greenfield A, Johnson K, Marks A, Nadal Ginard B, Brown S. Establishment of the mouse chromosome 7 region with homology to the myotonic dystrophy region of human chromosome 19q. Genomics. 1990;7:12-8 pubmed
    A number of genetic markers, including ATP1A3, TGFB, CKMM, and PRKCG, define the genetic region on human chromosome 19 containing the myotonic dystrophy locus...
  54. Ivandic B, Utz H, Kaczmarek P, Aherrahrou Z, Axtner S, Klepsch C, et al. New Dyscalc loci for myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice. Physiol Genomics. 2001;6:137-44 pubmed
    ..Additive epistasis between Dyscalc1 and Dyscalc2 enhanced DCC. Examining recombinant inbred strains, we propose a 10-cM interval containing Dyscalc1 and discuss potential candidate genes...
  55. Messina G, Biressi S, Monteverde S, Magli A, Cassano M, Perani L, et al. Nfix regulates fetal-specific transcription in developing skeletal muscle. Cell. 2010;140:554-66 pubmed publisher 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...
  56. Valdez M, Richardson J, Klein W, Olson E. Failure of Myf5 to support myogenic differentiation without myogenin, MyoD, and MRF4. Dev Biol. 2000;219:287-98 pubmed
  57. Katz A, Andersson D, Yu J, Norman B, Sandstrom M, Wieringa B, et al. Contraction-mediated glycogenolysis in mouse skeletal muscle lacking creatine kinase: the role of phosphorylase b activation. J Physiol. 2003;553:523-31 pubmed
    ..These data indicate that allosteric activation of phosphorylase b accounts for the accelerated glycogenolysis in CK-/- muscle during contraction. ..
  58. Guevara Fujita M, Loechel R, Venta P, Yuzbasiyan Gurkan V, Brewer G. Chromosomal assignment of seven genes on canine chromosomes by fluorescence in situ hybridization. Mamm Genome. 1996;7:268-70 pubmed
    ..These assignments are based on the karyotype proposed by Stone and associates (Genome 34, 407, 1991) using high-resolution techniques. In addition, we have assigned the Menkes gene to the X Chr of the dog. ..
  59. Ohkawa Y, Marfella C, Imbalzano A. Skeletal muscle specification by myogenin and Mef2D via the SWI/SNF ATPase Brg1. EMBO J. 2006;25:490-501 pubmed
  60. Nahrendorf M, Spindler M, Hu K, Bauer L, Ritter O, Nordbeck P, et al. Creatine kinase knockout mice show left ventricular hypertrophy and dilatation, but unaltered remodeling post-myocardial infarction. Cardiovasc Res. 2005;65:419-27 pubmed
    ..Mito-CK-/- and M/Mito-CK-/- mice show significant LV dilatation and marked LV hypertrophy, but LV remodeling post-MI is not aggravated. CK ablation leads to substantial adaptational changes in heart. ..
  61. Himeda C, Ranish J, Angello J, Maire P, Aebersold R, Hauschka S. Quantitative proteomic identification of six4 as the trex-binding factor in the muscle creatine kinase enhancer. Mol Cell Biol. 2004;24:2132-43 pubmed
    Transcriptional regulatory element X (Trex) is a positive control site within the Muscle creatine kinase (MCK) enhancer...
  62. Lu J, Webb R, Richardson J, Olson E. MyoR: a muscle-restricted basic helix-loop-helix transcription factor that antagonizes the actions of MyoD. Proc Natl Acad Sci U S A. 1999;96:552-7 pubmed
    ..These results suggest a role for MyoR as a lineage-restricted transcriptional repressor of the muscle differentiation program. ..
  63. van Deursen J, Jap P, Heerschap A, ter Laak H, Ruitenbeek W, Wieringa B. Effects of the creatine analogue beta-guanidinopropionic acid on skeletal muscles of mice deficient in muscle creatine kinase. Biochim Biophys Acta. 1994;1185:327-35 pubmed
    ..Altogether, these results provide evidence that certain functions of the creatine kinase/phosphocreatine (CK/PCr) system are not eliminated solely by the loss of M-CK. ..
  64. Yamane A, Ohnuki Y, Saeki Y. Delayed embryonic development of mouse masseter muscle correlates with delayed MyoD family expression. J Dent Res. 2000;79:1933-6 pubmed
    ..These results suggest that the delayed expression of the myoD family genes in the masseter correlates with delayed differentiation and maturation, probably due to the later functional requirements of the masseter than of the tongue. ..
  65. Warren G, O farrell L, Rogers K, Billings K, Sayers S, Clarkson P. CK-MM autoantibodies: prevalence, immune complexes, and effect on CK clearance. Muscle Nerve. 2006;34:335-46 pubmed
    ..Thus, the relatively low blood CK levels seen in some individuals following injury may be attributed partly or entirely to an autoantibody-enhanced clearance of CK...
  66. van Deursen J, Ruitenbeek W, Heerschap A, Jap P, ter Laak H, Wieringa B. Creatine kinase (CK) in skeletal muscle energy metabolism: a study of mouse mutants with graded reduction in muscle CK expression. Proc Natl Acad Sci U S A. 1994;91:9091-5 pubmed
    ..The ability of muscles to perform burst activity is also subnormal and closely correlates with the level of M-CK expression. ..
  67. Ventura Clapier R, Kuznetsov A, d Albis A, van Deursen J, Wieringa B, Veksler V. Muscle creatine kinase-deficient mice. I. Alterations in myofibrillar function. J Biol Chem. 1995;270:19914-20 pubmed
    ..These results show that no fundamental remodelling occurs in myofibrils of transgenic animals but that important adaptations modify the bioenergetic pathways including glycolytic metabolism. ..
  68. Rawls A, Morris J, Rudnicki M, Braun T, Arnold H, Klein W, et al. Myogenin's functions do not overlap with those of MyoD or Myf-5 during mouse embryogenesis. Dev Biol. 1995;172:37-50 pubmed
    ..These results demonstrate that the functions of myogenin do not overlap with those of MyoD or Myf-5 and support the view that myogenin acts in a genetic pathway downstream of MyoD and Myf-5. ..
  69. Lyons G, Muhlebach S, Moser A, Masood R, Paterson B, Buckingham M, et al. Developmental regulation of creatine kinase gene expression by myogenic factors in embryonic mouse and chick skeletal muscle. Development. 1991;113:1017-29 pubmed
    ..In the mouse, BCK transcript levels fall of rapidly in striated muscle shortly after the onset of MCK gene expression...
  70. Takahashi C, Bronson R, Socolovsky M, Contreras B, Lee K, Jacks T, et al. Rb and N-ras function together to control differentiation in the mouse. Mol Cell Biol. 2003;23:5256-68 pubmed
    ..Additionally, Rb(-/-); N-ras(-/-) muscle shows a restoration in the expression of the late muscle-specific gene MCK, and this correlates with a significant potentiation of MyoD transcriptional activity in Rb(-/-); N-ras(-/-), ..
  71. Rudert F, Saunders A, Rebstock S, Thompson J, Zimmermann W. Characterization of murine carcinoembryonic antigen gene family members. Mamm Genome. 1992;3:262-73 pubmed
    ..The more distantly related Cea-5 seems to be ubiquitously expressed. The putative promoter region of Cea-2 lacks typical TATA- or CAAT-boxes, but contains other conserved motifs that could play a role in the initiation of transcription. ..