COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE

COMPENSATION FOR IMPAIRED MYOCARDIAL PHOSPHOTRANSFER IN GUANIDINOACETATE-N-METHYLTRANSFERASE KNOCKOUT MICE

מידע ביבליוגרפי
Main Authors:	Aksentijevic, D, Lygate, C, Makinen, K, Sebag-Montefiore, L, Medway, D, Neubauer, S
פורמט:	Conference item
יצא לאור:	2010

פריטים דומים

GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
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Adaptations to Maintain Energy Homeostasis Compensate for Creatine-Deficiency in GAMT Knockout Mice Following Myocardial Infarction, but May Contribute to Early Mitochondrial Pathology During Aging
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Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age.
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Impaired cardiac contractile function in AGAT knockout mice devoid of creatine is rescued by homoarginine but not creatine
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Ribose Supplementation Alone or with Elevated Creatine Does Not Preserve High Energy Nucleotides or Cardiac Function in the Failing Mouse Heart.
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Regulation of myocardial creatine uptake capacity in genetically altered mouse models
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Phosphotransfer in Rhodobacter sphaeroides chemotaxis.
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