Presenilins are Essential for Regulating Neurotransmitter Release

[1]  R. J. Kelleher,et al.  Indirect Regulation of Presenilins in CREB-mediated Transcription* , 2009, Journal of Biological Chemistry.

[2]  Ian Parker,et al.  SERCA pump activity is physiologically regulated by presenilin and regulates amyloid beta production. , 2008, The Journal of general physiology.

[3]  F. LaFerla,et al.  SERCA pump activity is physiologically regulated by presenilin and regulates amyloid β production , 2008, The Journal of cell biology.

[4]  Douglas R. Porter,et al.  Impaired dopamine release and synaptic plasticity in the striatum of PINK1-deficient mice , 2007, Proceedings of the National Academy of Sciences.

[5]  R. J. Kelleher,et al.  The presenilin hypothesis of Alzheimer's disease: Evidence for a loss-of-function pathogenic mechanism , 2007, Proceedings of the National Academy of Sciences.

[6]  B. Strooper,et al.  Presenilins Form ER Ca2+ Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations , 2006, Cell.

[7]  F. LaFerla,et al.  Enhanced Ryanodine Receptor Recruitment Contributes to Ca2+ Disruptions in Young, Adult, and Aged Alzheimer's Disease Mice , 2006, The Journal of Neuroscience.

[8]  P. Greengard,et al.  Regulation of NMDA receptor trafficking by amyloid-β , 2005, Nature Neuroscience.

[9]  R. Morris,et al.  Conditional Inactivation of Presenilin 1 Prevents Amyloid Accumulation and Temporarily Rescues Contextual and Spatial Working Memory Impairments in Amyloid Precursor Protein Transgenic Mice , 2005, The Journal of Neuroscience.

[10]  P. Calabresi,et al.  Nigrostriatal Dopaminergic Deficits and Hypokinesia Caused by Inactivation of the Familial Parkinsonism-Linked Gene DJ-1 , 2005, Neuron.

[11]  Jie Shen,et al.  Role of presenilin-1 in cortical lamination and survival of Cajal-Retzius neurons. , 2005, Developmental biology.

[12]  P. Greengard,et al.  Regulation of NMDA receptor trafficking by amyloid-beta. , 2005, Nature neuroscience.

[13]  J. Tsien,et al.  Forebrain degeneration and ventricle enlargement caused by double knockout of Alzheimer's presenilin-1 and presenilin-2. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[14]  E. Kandel,et al.  Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration , 2004, Neuron.

[15]  Grace E Stutzmann,et al.  Dysregulated IP3 Signaling in Cortical Neurons of Knock-In Mice Expressing an Alzheimer's-Linked Mutation in Presenilin1 Results in Exaggerated Ca2+ Signals and Altered Membrane Excitability , 2004, The Journal of Neuroscience.

[16]  E. Kandel,et al.  Presynaptic BDNF Required for a Presynaptic but Not Postsynaptic Component of LTP at Hippocampal CA1-CA3 Synapses , 2003, Neuron.

[17]  R. Malinow,et al.  APP Processing and Synaptic Function , 2003, Neuron.

[18]  D. Peterson,et al.  Evidence That Synaptically Released β-Amyloid Accumulates as Extracellular Deposits in the Hippocampus of Transgenic Mice , 2002, The Journal of Neuroscience.

[19]  D. Selkoe.  Alzheimer's Disease Is a Synaptic Failure , 2002, Science.

[20]  J. Hardy,et al.  The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .

[21]  M. Quirk,et al.  Requirement for Hippocampal CA3 NMDA Receptors in Associative Memory Recall , 2002, Science.

[22]  Chen Zhang,et al.  Ca2+-independent but voltage-dependent secretion in mammalian dorsal root ganglion neurons , 2002, Nature Neuroscience.

[23]  C. Zhang,et al.  Ca(2+)-independent but voltage-dependent secretion in mammalian dorsal root ganglion neurons. , 2002, Nature neuroscience.

[24]  E. Kandel,et al.  APP Processing and Synaptic Plasticity in Presenilin-1 Conditional Knockout Mice , 2001, Neuron.

[25]  Alan Fine,et al.  Calcium Stores in Hippocampal Synaptic Boutons Mediate Short-Term Plasticity, Store-Operated Ca2+ Entry, and Spontaneous Transmitter Release , 2001, Neuron.

[26]  M. Mattson,et al.  Presenilin-1 Mutations Increase Levels of Ryanodine Receptors and Calcium Release in PC12 Cells and Cortical Neurons* , 2000, The Journal of Biological Chemistry.

[27]  M. Handler,et al.  Presenilin-1 regulates neuronal differentiation during neurogenesis. , 2000, Development.

[28]  S. Lincoln,et al.  A Loss of Function Mutation of Presenilin-2 Interferes with Amyloid β-Peptide Production and Notch Signaling* , 1999, The Journal of Biological Chemistry.

[29]  R. Nicoll,et al.  Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[30]  J. Buxbaum,et al.  Alzheimer Amyloid Protein Precursor in the Rat Hippocampus: Transport and Processing through the Perforant Path , 1998, The Journal of Neuroscience.

[31]  S. Christensen,et al.  A tool coming of age: thapsigargin as an inhibitor of sarco-endoplasmic reticulum Ca(2+)-ATPases. , 1998, Trends in pharmacological sciences.

[32]  T. Molinski,et al.  Xestospongins: Potent Membrane Permeable Blockers of the Inositol 1,4,5-Trisphosphate Receptor , 1997, Neuron.

[33]  S. Tonegawa,et al.  Skeletal and CNS Defects in Presenilin-1-Deficient Mice , 1997, Cell.

[34]  R. Malinow,et al.  The probability of transmitter release at a mammalian central synapse , 1993, Nature.

[35]  Christian Rosenmund,et al.  Nonuniform probability of glutamate release at a hippocampal synapse. , 1993, Science.

[36]  G. Meissner,et al.  Ryanodine activation and inhibition of the Ca2+ release channel of sarcoplasmic reticulum. , 1986, The Journal of biological chemistry.