Mechanism of cytotoxicity mediated by the C31 fragment of the amyloid precursor protein.

[1]  S. Heinemann,et al.  Deficits in Synaptic Transmission and Learning in Amyloid Precursor Protein (APP) Transgenic Mice Require C-Terminal Cleavage of APP , 2006, The Journal of Neuroscience.

[2]  D. Bredesen,et al.  Aβ induces cell death by direct interaction with its cognate extracellular domain on APP (APP 597–624) , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[3]  D. Bredesen,et al.  Correction for Galvan et al., Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664 , 2006, Proceedings of the National Academy of Sciences.

[4]  A. Prochiantz,et al.  SET protein (TAF1β, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain , 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[5]  D. Bredesen,et al.  Caspase cleavage of the amyloid precursor protein modulates amyloid β‐protein toxicity , 2003, Journal of neurochemistry.

[6]  Y. Suh,et al.  C‐terminal fragments of amyloid precursor protein exert neurotoxicity by inducing glycogen synthase kinase‐3β expression , 2003 .

[7]  Bradley T. Hyman,et al.  The gamma secretase-generated carboxyl-terminal domain of the amyloid precursor protein induces apoptosis via Tip60 in H4 cells. , 2002, The Journal of biological chemistry.

[8]  D. Bredesen,et al.  Caspase cleavage of members of the amyloid precursor family of proteins , 2002, Journal of neurochemistry.

[9]  A. Prochiantz,et al.  A Short Cytoplasmic Domain of the Amyloid Precursor Protein Induces Apoptosis In Vitro and In Vivo , 2001, Molecular and Cellular Neuroscience.

[10]  S. Chandra,et al.  The Amyloidogenic Pathway of Amyloid Precursor Protein (APP) Is Independent of Its Cleavage by Caspases* , 2001, The Journal of Biological Chemistry.

[11]  D. Selkoe Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.

[12]  S. Chandra,et al.  A second cytotoxic proteolytic peptide derived from amyloid β-protein precursor , 2000, Nature Medicine.

[13]  Michelle Palmer,et al.  Epidermal growth factor receptor dimerization monitored in live cells , 2000, Nature Biotechnology.

[14]  David Smith,et al.  Involvement of Caspases in Proteolytic Cleavage of Alzheimer’s Amyloid-β Precursor Protein and Amyloidogenic Aβ Peptide Formation , 1999, Cell.

[15]  H. Ninomiya,et al.  Secreted Form of Amyloid β/A4 Protein Precursor (APP) Binds to Two Distinct APP Binding Sites on Rat B103 Neuron‐Like Cells Through Two Different Domains, but Only One Site Is Involved in Neuritotropic Activity , 1994, Journal of neurochemistry.

[16]  D. Salmon,et al.  Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment , 1991, Annals of neurology.

[17]  G. Multhaup,et al.  GxxxG motifs within the amyloid precursor protein transmembrane sequence are critical for the etiology of Abeta42. , 2007, The EMBO journal.

[18]  S. Chandra,et al.  A second cytotoxic proteolytic peptide derived from amyloid beta-protein precursor. , 2000, Nature medicine.

[19]  G. Robertson,et al.  Involvement of caspases in proteolytic cleavage of Alzheimer's amyloid-beta precursor protein and amyloidogenic A beta peptide formation. , 1999, Cell.