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

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

Opis bibliograficzny
Główni autorzy:	Aksentijevic, D, Lygate, C, Makinen, K, Sebag-Montefiore, L, Medway, D, Neubauer, S
Format:	Conference item
Wydane:	2010

Podobne zapisy

GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
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Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.
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Cardiac structure and function during ageing in energetically compromised Guanidinoacetate N-methyltransferase (GAMT)-knockout mice – a one year longitudinal MRI study
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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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Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction.
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Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics
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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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Cardiac dysfunction and peri-weaning mortality in malonyl-coenzyme A decarboxylase (MCD) knockout mice as a consequence of restricting substrate plasticity.
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Living without creatine: unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice.
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Regulation of Myocardial Creatine Uptake by Intra- and Extracellular Creatine Levels
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Regulation of myocardial creatine uptake capacity in genetically altered mouse models
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Processing mechanism of guanidinoacetate in choroid plexus epithelial cells: conversion of guanidinoacetate to creatine via guanidinoacetate N-methyltransferase and monocarboxylate transporter 12-mediated creatine release into the CSF
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Complete absence of creatine but unaltered ATP levels in hearts from AGAT knockout mice
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Guanidinoacetate N-methyltransferase deficiency: Case report and brief review of the literature
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od: Vinu Narayan, i wsp.
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A role for thioredoxin-interacting protein (Txnip) in cellular creatine homeostasis.
od: Zervou, S, i wsp.
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REGULATION OF CELLULAR CREATINE HOMEOSTASIS: A ROLE FOR THIOREDOXIN INTERACTING PROTEIN (TXNIP)
od: Zervou, S, i wsp.
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Phosphotransfer in Rhodobacter sphaeroides chemotaxis.
od: Porter, S, i wsp.
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Severely altered guanidino compound levels, disturbed body weight homeostasis and impaired fertility in a mouse model of guanidinoacetate N-methyltransferase (GAMT) deficiency.
od: Schmidt, A, i wsp.
Wydane: (2004)

A novel mutation in two cousins with guanidinoacetate methyltransferase (GAMT) deficiency presented with autism
od: Halil İbrahim Aydın, i wsp.
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Guanidinoacetate methyltransferase deficiency: A treatable cause of developmental delay diagnosed by magnetic resonance spectroscopy
od: L Caroline Silvia, i wsp.
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Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
od: Phillips, D, i wsp.
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The creatine kinase energy transport system in the failing mouse heart
od: Lygate, C, i wsp.
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Accelerating global left-ventricular function assessment in mice using reduced slice acquisition and three-dimensional guide-point modelling.
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