Presenilins, APP, and Notch: Proteolysis from Womb to Tomb

[1]  F. D. Miller,et al.  Functional gamma‐secretase inhibitors reduce beta‐amyloid peptide levels in brain , 2000, Journal of neurochemistry.

[2]  P. Fraser,et al.  Mutation of conserved aspartates affects maturation of both aspartate mutant and endogenous presenilin 1 and presenilin 2 complexes. , 2000, The Journal of biological chemistry.

[3]  Graeme Irvine Stevenson,et al.  L-685,458, an Aspartyl Protease Transition State Mimic, Is a Potent Inhibitor of Amyloid β-Protein Precursor γ-Secretase Activity , 2000 .

[4]  D. Selkoe,et al.  Transition-state analogue inhibitors of γ-secretase bind directly to presenilin-1 , 2000, Nature Cell Biology.

[5]  B. Strooper,et al.  Total inactivation of γ–secretase activity in presenilin-deficient embryonic stem cells , 2000, Nature Cell Biology.

[6]  A. Bernstein,et al.  Presenilins are required for γ-secretase cleavage of β-APP and transmembrane cleavage of Notch-1 , 2000, Nature Cell Biology.

[7]  Raphael Kopan,et al.  Embryonic lethality in mice homozygous for a processing-deficient allele of Notch1 , 2000, Nature.

[8]  Min Xu,et al.  Photoactivated γ-secretase inhibitors directed to the active site covalently label presenilin 1 , 2000, Nature.

[9]  Min Xu,et al.  Presenilin 1 is linked with gamma-secretase activity in the detergent solubilized state. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[10]  S. Artavanis-Tsakonas,et al.  Notch signaling and the determination of appendage identity. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[11]  D. Selkoe,et al.  The Transmembrane Aspartates in Presenilin 1 and 2 Are Obligatory for γ-Secretase Activity and Amyloid β-Protein Generation* , 2000, The Journal of Biological Chemistry.

[12]  A Cumano,et al.  A novel proteolytic cleavage involved in Notch signaling: the role of the disintegrin-metalloprotease TACE. , 2000, Molecular cell.

[13]  D. Selkoe,et al.  Notch and presenilins in vertebrates and invertebrates: implications for neuronal development and degeneration , 2000, Current Opinion in Neurobiology.

[14]  Raphael Kopan,et al.  A ligand-induced extracellular cleavage regulates gamma-secretase-like proteolytic activation of Notch1. , 2000, Molecular cell.

[15]  M. Citron,et al.  Amyloidogenic function of the Alzheimer's disease-associated presenilin 1 in the absence of endoproteolysis. , 1999, Biochemistry.

[16]  A. Bernstein,et al.  Mice lacking both presenilin genes exhibit early embryonic patterning defects. , 1999, Genes & development.

[17]  H. Vanderstichele,et al.  Presenilin 2 deficiency causes a mild pulmonary phenotype and no changes in amyloid precursor protein processing but enhances the embryonic lethal phenotype of presenilin 1 deficiency. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[18]  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.

[19]  G. Boulianne,et al.  Drosophila presenilin Is Required for Neuronal Differentiation and Affects Notch Subcellular Localization and Signaling , 1999, The Journal of Neuroscience.

[20]  Toshiki Nakai,et al.  Membrane Topology of Alzheimer’s Disease-related Presenilin 1 , 1999, The Journal of Biological Chemistry.

[21]  D. Selkoe,et al.  Translating cell biology into therapeutic advances in Alzheimer's disease , 1999, Nature.

[22]  D. Selkoe,et al.  Peptidomimetic probes and molecular modeling suggest that Alzheimer's gamma-secretase is an intramembrane-cleaving aspartyl protease. , 1999, Biochemistry.

[23]  D. Selkoe,et al.  Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity , 1999, Nature.

[24]  William J. Ray,et al.  A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain , 1999, Nature.

[25]  K. Beyreuther,et al.  Mechanism of the cleavage specificity of Alzheimer's disease gamma-secretase identified by phenylalanine-scanning mutagenesis of the transmembrane domain of the amyloid precursor protein. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[26]  R. Wang,et al.  アミロイド前駆体蛋白質の貫通膜領域のフェニルアラニン‐走査突然変異誘発により確認されたアルツハイマー病γ‐セクレターゼの切断特異性の機序 , 1999 .

[27]  P. Kloetzel,et al.  Expression of Alzheimer’s Disease-associated Presenilin-1 Is Controlled by Proteolytic Degradation and Complex Formation* , 1998, The Journal of Biological Chemistry.

[28]  I. Greenwald,et al.  Additional evidence for an eight-transmembrane-domain topology for Caenorhabditis elegans and human presenilins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[29]  Raphael Kopan,et al.  Notch-1 signalling requires ligand-induced proteolytic release of intracellular domain , 1998, Nature.

[30]  C. Flexner.  HIV-protease inhibitors. , 1998, The New England journal of medicine.

[31]  D. Selkoe,et al.  The Proteolytic Fragments of the Alzheimer’s Disease-associated Presenilin-1 Form Heterodimers and Occur as a 100–150-kDa Molecular Mass Complex* , 1998, The Journal of Biological Chemistry.

[32]  C. L. Harris,et al.  Stable Association of Presenilin Derivatives and Absence of Presenilin Interactions with APP , 1998, Neurobiology of Disease.

[33]  Hugo Vanderstichele,et al.  Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.

[34]  D. Selkoe,et al.  A Substrate-Based Difluoro Ketone Selectively Inhibits Alzheimer's γ-Secretase Activity , 1998 .

[35]  R. Sherrington,et al.  Presenilin Proteins Undergo Heterogeneous Endoproteolysis between Thr291and Ala299and Occur as Stable N- and C-Terminal Fragments in Normal and Alzheimer Brain Tissue , 1997, Neurobiology of Disease.

[36]  G. Multhaup,et al.  Mutations in the transmembrane domain of APP altering gamma-secretase specificity. , 1997, Biochemistry.

[37]  C. L. Harris,et al.  Evidence That Levels of Presenilins (PS1 and PS2) Are Coordinately Regulated by Competition for Limiting Cellular Factors* , 1997, The Journal of Biological Chemistry.

[38]  D. Borchelt,et al.  Endoproteolytic Processing and Stabilization of Wild-type and Mutant Presenilin* , 1997, The Journal of Biological Chemistry.

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

[40]  D. Price,et al.  Presenilin 1 is required for Notch 1 and Dll1 expression in the paraxial mesoderm , 1997, Nature.

[41]  D. Harris,et al.  Evidence for a Six-transmembrane Domain Structure of Presenilin 1* , 1997, The Journal of Biological Chemistry.

[42]  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.

[43]  J. Hardy,et al.  The Alzheimer family of diseases: many etiologies, one pathogenesis? , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[44]  I. Greenwald,et al.  Membrane Topology of the C. elegans SEL-12 Presenilin , 1996, Neuron.

[45]  D. Borchelt,et al.  Protein Topology of Presenilin 1 , 1996, Neuron.

[46]  T. Iwatsubo,et al.  Familial Alzheimer's disease-linked mutations at Val717 of amyloid precursor protein are specific for the increased secretion of A beta 42(43). , 1996, Biochemical and biophysical research communications.

[47]  E. Tischer,et al.  Beta-amyloid precursor protein. Location of transmembrane domain and specificity of gamma-secretase cleavage. , 1996, The Journal of biological chemistry.

[48]  D. Borchelt,et al.  Endoproteolysis of Presenilin 1 and Accumulation of Processed Derivatives In Vivo , 1996, Neuron.

[49]  R E Cachau,et al.  Inhibition and catalytic mechanism of HIV-1 aspartic protease. , 1996, Journal of molecular biology.

[50]  J. Rommens,et al.  Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene , 1995, Nature.

[51]  G. Schellenberg,et al.  Candidate gene for the chromosome 1 familial Alzheimer's disease locus , 1995, Science.

[52]  D. Pollen,et al.  Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease , 1995, Nature.

[53]  R A Mueller,et al.  Discovery of a novel class of potent HIV-1 protease inhibitors containing the (R)-(hydroxyethyl)urea isostere. , 1993, Journal of medicinal chemistry.

[54]  D. Veber,et al.  Cyclic peptides as selective tachykinin antagonists. , 1993, Journal of medicinal chemistry.

[55]  Michael H. Gelb,et al.  Crystallographic analysis of transition state mimics bound to penicillopepsin: difluorostatine- and difluorostatone-containing peptides. , 1994 .

[56]  T L Blundell,et al.  Direct observation by X‐ray analysis of the tetrahedral “intermediate” of aspartic proteinases , 1992, Protein science : a publication of the Protein Society.

[57]  A. Doherty,et al.  Design and synthesis of potent, selective, and orally active fluorine-containing renin inhibitors. , 1992, Journal of medicinal chemistry.

[58]  W. Watt,et al.  Design and synthesis of potent and specific renin inhibitors containing difluorostatine, difluorostatone, and related analogues. , 1986, Journal of medicinal chemistry.