Modeling Clinically Heterogeneous Presenilin Mutations with Transgenic Drosophila

[1]  M. Doran,et al.  Clinical phenotypic heterogeneity of Alzheimer's disease associated with mutations of the presenilin–1 gene , 2006, Journal of Neurology.

[2]  B. Miller,et al.  Presenilin 1 Glu318Gly polymorphism: interpret with caution. , 2005, Archives of neurology.

[3]  J. Schröder,et al.  Mean age of onset in familial Alzheimer's disease is determined by amyloid beta 42 , 2005, Neurobiology of Aging.

[4]  A. Goate,et al.  Presenilin function and γ‐secretase activity , 2005, Journal of neurochemistry.

[5]  M. Wolfe,et al.  Intramembrane Proteolysis: Theme and Variations , 2004, Science.

[6]  L. Baki,et al.  PS1 activates PI3K thus inhibiting GSK‐3 activity and tau overphosphorylation: effects of FAD mutations , 2004, The EMBO journal.

[7]  P. Marambaud,et al.  Genetic and molecular aspects of Alzheimer's disease shed light on new mechanisms of transcriptional regulation , 2004, Genes, brain, and behavior.

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

[9]  J. Shioi,et al.  A CBP Binding Transcriptional Repressor Produced by the PS1/ϵ-Cleavage of N-Cadherin Is Inhibited by PS1 FAD Mutations , 2003, Cell.

[10]  F. Panza,et al.  F175S Change and a Novel Polymorphism in Presenilin-1 Gene in Late-Onset Familial Alzheimer’s Disease , 2002, European Neurology.

[11]  S. Artavanis-Tsakonas,et al.  Notch Signaling : Cell Fate Control and Signal Integration in Development , 1999 .

[12]  T. Iwatsubo,et al.  Enhancement of amyloid β 42 secretion by 28 different presenilin 1 mutations of familial Alzheimer's disease , 1999, Neuroscience Letters.

[13]  Iva Greenwald,et al.  Presenilin is required for activity and nuclear access of Notch in Drosophila , 1999, Nature.

[14]  M. Fortini,et al.  Neurogenic phenotypes and altered Notch processing in Drosophila Presenilin mutants , 1999, Nature.

[15]  D. Selkoe,et al.  The cell biology of β-amyloid precursor protein and presenilin in Alzheimer's disease , 1998 .

[16]  D. Borchelt,et al.  An Alzheimer's Disease-Linked PS1 Variant Rescues the Developmental Abnormalities of PS1-Deficient Embryos , 1998, Neuron.

[17]  Gurparkash Singh,et al.  Mutant Human Presenilin 1 Protects presenilin 1 Null Mouse against Embryonic Lethality and Elevates Aβ1–42/43 Expression , 1998, Neuron.

[18]  J. Hardy,et al.  Increased Aβ42(43) from cell lines expressing presenilin 1 mutations , 1998, Annals of neurology.

[19]  C. Haass,et al.  Human presenilin-1, but not familial Alzheimer's disease (FAD) mutants, facilitate Caenorhabditis elegans Notch signalling independently of proteolytic processing. , 1997, Genes and function.

[20]  I. Greenwald,et al.  Assessment of normal and mutant human presenilin function in Caenorhabditis elegans. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[21]  A. Bang,et al.  Direct downstream targets of proneural activators in the imaginal disc include genes involved in lateral inhibitory signaling. , 1994, Genes & development.

[22]  T. Tully,et al.  Human amyloid precursor protein ameliorates behavioral deficit of flies deleted for appl gene , 1992, Neuron.

[23]  C. Klämbt,et al.  Closely related transcripts encoded by the neurogenic gene complex enhancer of split of Drosophila melanogaster. , 1989, The EMBO journal.

[24]  S. Siegel,et al.  Nonparametric Statistics for the Behavioral Sciences , 2022, The SAGE Encyclopedia of Research Design.

[25]  A. Hofman,et al.  The Glu318Gly substitution in presenilin 1 is not causally related to Alzheimer disease. , 1999, American journal of human genetics.