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

التفاصيل البيبلوغرافية
المؤلفون الرئيسيون:	Aksentijevic, D, Lygate, C, Makinen, K, Sebag-Montefiore, L, Medway, D, Neubauer, S
التنسيق:	Conference item
منشور في:	2010

GUANIDINOACETATE N-METHYLTRANSFERASE KNOCKOUT MICE EXHIBIT NORMAL LEFT VENTRICULAR REMODELLING, HAEMODYNAMICS AND SURVIVAL AFTER MYOCARDIAL INFARCTION DESPITE LACK OF PHOSPHOCREATINE
حسب: Lygate, C, وآخرون
منشور في: (2010)

High energy phosphotransfer in the failing mouse heart-role of adenylate kinase and glycolytic enzymes
حسب: Aksentijevic, D, وآخرون
منشور في: (2010)

High-energy phosphotransfer in the failing mouse heart: role of adenylate kinase and glycolytic enzymes.
حسب: Aksentijević, D, وآخرون
منشور في: (2010)

Age-dependent decline in cardiac function in guanidinoacetate-N-methyltransferase knockout mice
حسب: Aksentijević, D, وآخرون
منشور في: (2019)

Age-Dependent Decline in Cardiac Function in Guanidinoacetate-N-Methyltransferase Knockout Mice
حسب: Dunja Aksentijević, وآخرون
منشور في: (2020-01-01)

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
حسب: Lygate, C, وآخرون
منشور في: (2011)

Guanidinoacetate N-methyltransferase-knockout mice completely lacking myocardial phosphocreatine show normal in vivo cardiac function, but increased susceptibility to ischemia/reperfusion injury
حسب: Lygate, C, وآخرون
منشور في: (2004)

Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout mice.
حسب: ten Hove, M, وآخرون
منشور في: (2005)

Metabolic Inflexibility of Malonyl CoA Decarboxylase (MCD) Knockout Mice Leads to Cardiac Remodelling and High Mortality During Peri-Weaning Period
حسب: Aksentijevic, D, وآخرون
منشور في: (2014)

Cardiac structure and function during ageing in energetically compromised Guanidinoacetate N-methyltransferase (GAMT)-knockout mice - a one year longitudinal MRI study.
حسب: Schneider, J, وآخرون
منشور في: (2008)

Cardiac phenotype of mitochondrial creatine kinase knockout mice is modified on a pure C57BL/6 genetic background.
حسب: Lygate, C, وآخرون
منشور في: (2009)

Guanidinoacetate Methyltransferase Deficiency
حسب: Eduardo P. Marques, وآخرون
منشور في: (2016-10-01)

Cardiac structure and function during ageing in energetically compromised Guanidinoacetate N-methyltransferase (GAMT)-knockout mice – a one year longitudinal MRI study
حسب: Clarke Kieran, وآخرون
منشور في: (2008-02-01)

Ribose supplementation alone or with elevated creatine does not preserve high energy nucleotides or cardiac function in the failing mouse heart
حسب: Faller, K, وآخرون
منشور في: (2013)

Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction.
حسب: Lygate, C, وآخرون
منشور في: (2012)

Elevated Myocardial Creatine Protects Against Ischemia/Reperfusion Injury by Improving Cardiac Energetics
حسب: Lygate, C, وآخرون
منشور في: (2011)

Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age
حسب: Lygate, C, وآخرون
منشور في: (2012)

Chronic creatine kinase deficiency eventually leads to congestive heart failure, but severity is dependent on genetic background, gender and age.
حسب: Lygate, C, وآخرون
منشور في: (2012)

Cardiac dysfunction and peri-weaning mortality in malonyl-coenzyme A decarboxylase (MCD) knockout mice as a consequence of restricting substrate plasticity.
حسب: Aksentijević, D, وآخرون
منشور في: (2014)

Living without creatine: Unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice
حسب: Lygate, C, وآخرون
منشور في: (2013)

Living without creatine: unchanged exercise capacity and response to chronic myocardial infarction in creatine-deficient mice.
حسب: Lygate, C, وآخرون
منشور في: (2013)

Regulation of Myocardial Creatine Uptake by Intra- and Extracellular Creatine Levels
حسب: Makinen, K, وآخرون
منشور في: (2008)

Mild guanidinoacetate increase under partial guanidinoacetate methyltransferase deficiency strongly affects brain cell development
حسب: Layane Hanna-El-Daher, وآخرون
منشور في: (2015-07-01)

Impaired cardiac contractile function in AGAT knockout mice devoid of creatine is rescued by homoarginine but not creatine
حسب: Faller, K, وآخرون
منشور في: (2017)

Ribose Supplementation Alone or with Elevated Creatine Does Not Preserve High Energy Nucleotides or Cardiac Function in the Failing Mouse Heart.
حسب: Kiterie M E Faller, وآخرون
منشور في: (2013-01-01)

Regulation of myocardial creatine uptake capacity in genetically altered mouse models
حسب: Ten Hove, M, وآخرون
منشور في: (2007)

Gene therapy for guanidinoacetate methyltransferase deficiency restores cerebral and myocardial creatine while resolving behavioral abnormalities
حسب: Suhail Khoja, وآخرون
منشور في: (2022-06-01)

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
حسب: Ryuta Jomura, وآخرون
منشور في: (2022-06-01)

Complete absence of creatine but unaltered ATP levels in hearts from AGAT knockout mice
حسب: ten Hove, M, وآخرون
منشور في: (2007)

Guanidinoacetate N-methyltransferase deficiency: Case report and brief review of the literature
حسب: Joshua L. Libell, BS, وآخرون
منشور في: (2023-12-01)

Case series of creatine deficiency syndrome due to guanidinoacetate methyltransferase deficiency
حسب: Vinu Narayan, وآخرون
منشور في: (2020-01-01)

A role for thioredoxin-interacting protein (Txnip) in cellular creatine homeostasis.
حسب: Zervou, S, وآخرون
منشور في: (2013)

REGULATION OF CELLULAR CREATINE HOMEOSTASIS: A ROLE FOR THIOREDOXIN INTERACTING PROTEIN (TXNIP)
حسب: Zervou, S, وآخرون
منشور في: (2013)

Phosphotransfer in Rhodobacter sphaeroides chemotaxis.
حسب: Porter, S, وآخرون
منشور في: (2002)

Severely altered guanidino compound levels, disturbed body weight homeostasis and impaired fertility in a mouse model of guanidinoacetate N-methyltransferase (GAMT) deficiency.
حسب: Schmidt, A, وآخرون
منشور في: (2004)

A novel mutation in two cousins with guanidinoacetate methyltransferase (GAMT) deficiency presented with autism
حسب: Halil İbrahim Aydın, وآخرون
منشور في: (2019-02-01)

Guanidinoacetate methyltransferase deficiency: A treatable cause of developmental delay diagnosed by magnetic resonance spectroscopy
حسب: L Caroline Silvia, وآخرون
منشور في: (2022-01-01)

Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
حسب: Phillips, D, وآخرون
منشور في: (2010)

The creatine kinase energy transport system in the failing mouse heart
حسب: Lygate, C, وآخرون
منشور في: (2006)

Accelerating global left-ventricular function assessment in mice using reduced slice acquisition and three-dimensional guide-point modelling.
حسب: Young, A, وآخرون
منشور في: (2011)

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

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