siRNA against presenilin 1 (PS1) down regulates amyloid β42 production in IMR-32 cells

[1]  R. Kandimalla,et al.  siRNA against presenilin 1 (PS1) down regulates amyloid β42 production in IMR-32 cells , 2012, Journal of Biomedical Science.

[2]  M. Wolfe gamma-Secretase in biology and medicine. , 2009, Seminars in cell & developmental biology.

[3]  R. Vassar,et al.  The Role of Amyloid Precursor Protein Processing by BACE1, the β-Secretase, in Alzheimer Disease Pathophysiology* , 2008, Journal of Biological Chemistry.

[4]  M. Goedert,et al.  A Century of Alzheimer's Disease , 2006, Science.

[5]  R. Tanzi,et al.  Twenty Years of the Alzheimer’s Disease Amyloid Hypothesis: A Genetic Perspective , 2005, Cell.

[6]  B. Winblad,et al.  Co‐expressed presenilin 1 NTF and CTF form functional γ‐secretase complexes in cells devoid of full‐length protein , 2004, Journal of neurochemistry.

[7]  H. Paulson,et al.  Targeting Alzheimer's disease genes with RNA interference: an efficient strategy for silencing mutant alleles. , 2004, Nucleic acids research.

[8]  R. Bhatnagar,et al.  RNA Interference: Biology, Mechanism, and Applications , 2003, Microbiology and Molecular Biology Reviews.

[9]  Haibin Xia,et al.  Allele-specific silencing of dominant disease genes , 2003, Proceedings of the National Academy of Sciences of the United States of America.

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

[11]  C. Masters,et al.  A novel epsilon-cleavage within the transmembrane domain of the Alzheimer amyloid precursor protein demonstrates homology with Notch processing. , 2002, Biochemistry.

[12]  S. Younkin,et al.  Presenilins as therapeutic targets for the treatment of Alzheimer's disease. , 2001, Trends in molecular medicine.

[13]  Jun Xie,et al.  Prostate Apoptosis Response-4 Enhances Secretion of Amyloid β Peptide 1–42 in Human Neuroblastoma IMR-32 Cells by a Caspase-dependent Pathway* , 2001, The Journal of Biological Chemistry.

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

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

[16]  D. Selkoe,et al.  Transition-state analogue inhibitors of gamma-secretase bind directly to presenilin-1. , 2000, Nature cell biology.

[17]  A. Nadin,et al.  Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1. , 2000, Nature.

[18]  Alfredo G. Tomasselli,et al.  Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity , 1999, Nature.

[19]  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.

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

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

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

[23]  P. Fraser,et al.  The Presenilin 1 Protein Is a Component of a High Molecular Weight Intracellular Complex That Contains β-Catenin* , 1998, The Journal of Biological Chemistry.

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

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

[26]  D. Selkoe,et al.  A substrate-based difluoro ketone selectively inhibits Alzheimer's gamma-secretase activity. , 1998, Journal of medicinal chemistry.

[27]  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.

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

[29]  John Hardy,et al.  Amyloid, the presenilins and Alzheimer's disease , 1997, Trends in Neurosciences.

[30]  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.

[31]  G. Schellenberg,et al.  Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.

[32]  J. Hardy,et al.  Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease. , 1996, Nature medicine.