Murine Glut-1 transporter haploinsufficiency: Postnatal deceleration of brain weight and reactive astrocytosis

[1]  C. Metges,et al.  Technical note: Milk composition in mice--methodological aspects and effects of mouse strain and lactation day. , 2009, Journal of dairy science.

[2]  Calvin J Kuo,et al.  Wnt/β-catenin signaling is required for CNS, but not non-CNS, angiogenesis , 2009, Proceedings of the National Academy of Sciences.

[3]  James L. Park,et al.  A GSK-3/TSC2/mTOR pathway regulates glucose uptake and GLUT1 glucose transporter expression. , 2008, American journal of physiology. Cell physiology.

[4]  C. Ribak,et al.  Rapid astrocyte and microglial activation following pilocarpine‐induced seizures in rats , 2008, Epilepsia.

[5]  K. Guan,et al.  Expanding mTOR signaling , 2007, Cell Research.

[6]  Yuwu Jiang,et al.  Alterations of NR2B and PSD-95 expression after early-life epileptiform discharges in developing neurons , 2007, International Journal of Developmental Neuroscience.

[7]  J. Rathmell,et al.  Cytokine stimulation promotes glucose uptake via phosphatidylinositol-3 kinase/Akt regulation of Glut1 activity and trafficking. , 2007, Molecular biology of the cell.

[8]  C. Verney,et al.  Cortical Consequences of In Vivo Blockade of Monocarboxylate Transport During Brain Development in Mice , 2007, Pediatric Research.

[9]  M. Febbraio,et al.  AMP-activated protein kinase--the fat controller of the energy railroad. , 2006, Canadian journal of physiology and pharmacology.

[10]  R. Jope,et al.  The paradoxical pro- and anti-apoptotic actions of GSK3 in the intrinsic and extrinsic apoptosis signaling pathways , 2006, Progress in Neurobiology.

[11]  G. Ronnett,et al.  Developing a head for energy sensing: AMP‐activated protein kinase as a multifunctional metabolic sensor in the brain , 2006, The Journal of physiology.

[12]  Guido Gerig,et al.  User-guided 3D active contour segmentation of anatomical structures: Significantly improved efficiency and reliability , 2006, NeuroImage.

[13]  J. Gitlin,et al.  GLUT1 Deficiency Links Nutrient Availability and Apoptosis during Embryonic Development* , 2006, Journal of Biological Chemistry.

[14]  J. Noebels,et al.  A mouse model for Glut-1 haploinsufficiency. , 2006, Human molecular genetics.

[15]  P. Chan,et al.  Activation of the Akt/GSK3β Signaling Pathway Mediates Survival of Vulnerable Hippocampal Neurons after Transient Global Cerebral Ischemia in Rats , 2006 .

[16]  Luc Pellerin,et al.  Monocarboxylate transporters in the central nervous system: distribution, regulation and function , 2005, Journal of neurochemistry.

[17]  Hong Yang,et al.  Glut‐1 deficiency syndrome: Clinical, genetic, and therapeutic aspects , 2005, Annals of neurology.

[18]  P. Hammerman,et al.  Beginnings of a signal-transduction pathway for bioenergetic control of cell survival. , 2004, Trends in biochemical sciences.

[19]  N. Sonenberg,et al.  Upstream and downstream of mTOR. , 2004, Genes & development.

[20]  E. Faustman,et al.  The role of cell death during neocortical neurogenesis and synaptogenesis: implications from a computational model for the rat and mouse. , 2004, Brain research. Developmental brain research.

[21]  S. Dedhar,et al.  NGF-Induced Axon Growth Is Mediated by Localized Inactivation of GSK-3β and Functions of the Microtubule Plus End Binding Protein APC , 2004, Neuron.

[22]  R. Baggs,et al.  Glucose transporter-1-deficient mice exhibit impaired development and deformities that are similar to diabetic embryopathy , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[23]  S. Vannucci,et al.  Developmental switch in brain nutrient transporter expression in the rat. , 2003, American journal of physiology. Endocrinology and metabolism.

[24]  C. Verney,et al.  Perinatal and early postnatal changes in the expression of monocarboxylate transporters MCT1 and MCT2 in the rat forebrain , 2003, The Journal of comparative neurology.

[25]  Gregory L. Holmes,et al.  Seizure-induced neuronal injury: Animal data , 2002, Neurology.

[26]  B. Hyman,et al.  Neonatal neuronal overexpression of glycogen synthase kinase-3β reduces brain size in transgenic mice , 2002, Neuroscience.

[27]  P. Cohen,et al.  GSK3 takes centre stage more than 20 years after its discovery. , 2001, The Biochemical journal.

[28]  T. Boeckers,et al.  Kainate-induced seizures alter protein composition and N-methyl-d-aspartate receptor function of rat forebrain postsynaptic densities , 2001, Neuroscience.

[29]  K. Moley,et al.  Decreased Glucose Transporter Expression Triggers BAX-dependent Apoptosis in the Murine Blastocyst* , 2000, The Journal of Biological Chemistry.

[30]  R. McKnight,et al.  Developmental regulation of genes mediating murine brain glucose uptake. , 1999, American journal of physiology. Regulatory, integrative and comparative physiology.

[31]  Mark J. West,et al.  Stereological methods for estimating the total number of neurons and synapses: issues of precision and bias , 1999, Trends in Neurosciences.

[32]  D. Ferriero,et al.  Strain-related brain injury in neonatal mice subjected to hypoxia–ischemia , 1998, Brain Research.

[33]  T. Roberts,et al.  NB4S, a member of the TBC1 domain family of genes, is truncated as a result of a constitutional t(1;10)(p22;q21) chromosome translocation in a patient with stage 4S neuroblastoma. , 1998, Human molecular genetics.

[34]  P. Magistretti,et al.  Expression of monocarboxylate transporter mRNAs in mouse brain: support for a distinct role of lactate as an energy substrate for the neonatal vs. adult brain. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[35]  J. Parnavelas,et al.  Apoptosis and Its Relation to the Cell Cycle in the Developing Cerebral Cortex , 1997, The Journal of Neuroscience.

[36]  A. Blaschke,et al.  Widespread programmed cell death in proliferative and postmitotic regions of the fetal cerebral cortex. , 1996, Development.

[37]  S. Vannucci,et al.  Glucose transporter proteins in brain , 1994, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[38]  S. Harik,et al.  Defective glucose transport across the blood-brain barrier as a cause of persistent hypoglycorrhachia, seizures, and developmental delay. , 1991, The New England journal of medicine.

[39]  N. Copeland,et al.  Glucose transporter gene expression in early mouse embryos. , 1991, Development.

[40]  J. Ferrendelli,et al.  CHRONIC KETOSIS AND CEREBRAL METABOLISM , 1977, Pediatric Research.

[41]  G F Cahill,et al.  Brain metabolism during fasting. , 1967, The Journal of clinical investigation.