Chemical modifications of deposited amyloid-beta peptides.

[1]  S. Clarke,et al.  Membrane protein carboxyl methylation increases with human erythrocyte age. Evidence for an increase in the number of methylatable sites. , 1983, The Journal of biological chemistry.

[2]  S. Clarke,et al.  Synthetic peptide substrates for the erythrocyte protein carboxyl methyltransferase. Detection of a new site of methylation at isomerized L-aspartyl residues. , 1984, The Journal of biological chemistry.

[3]  D. Aswad Determination of D- and L-aspartate in amino acid mixtures by high-performance liquid chromatography after derivatization with a chiral adduct of o-phthaldialdehyde. , 1984, Analytical biochemistry.

[4]  S. Clarke,et al.  Age-dependent accumulation of protein residues which can be hydrolyzed to D-aspartic acid in human erythrocytes. , 1986, The Journal of biological chemistry.

[5]  S. Clarke,et al.  Protein carboxyl methyltransferase and methyl acceptor proteins in aging and cataractous tissue of the human eye lens , 1986, Mechanisms of Ageing and Development.

[6]  S. Clarke,et al.  Metabolism of a synthetic L-isoaspartyl-containing hexapeptide in erythrocyte extracts. Enzymatic methyl esterification is followed by nonenzymatic succinimide formation. , 1986, The Journal of biological chemistry.

[7]  S. Clarke,et al.  Deamidation, isomerization, and racemization at asparaginyl and aspartyl residues in peptides. Succinimide-linked reactions that contribute to protein degradation. , 1987, The Journal of biological chemistry.

[8]  R. Shapira,et al.  Differential racemization of aspartate and serine in human myelin basic protein. , 1987, Biochemical and biophysical research communications.

[9]  S. Capasso,et al.  Enzymatic methyl esterification of synthetic tripeptides: structural requirements of the peptide substrate. Detection of the reaction products by fast-atom-bombardment mass spectrometry. , 1988, European journal of biochemistry.

[10]  S. Clarke,et al.  Purification of homologous protein carboxyl methyltransferase isozymes from human and bovine erythrocytes. , 1988, Biochemistry.

[11]  S. Capasso,et al.  Enzymatic methyl esterification of synthetic tripeptides: structural requirements of the peptide substrate. Detection of the reaction products by fast-atom-bombardment mass spectrometry. , 1988 .

[12]  S. Mirra,et al.  Neuritic Plaque Amyloid in Alzheimer's Disease Is Highly Racemized , 1988, Journal of neurochemistry.

[13]  I. Ota,et al.  Enzymatic methylation of L-isoaspartyl residues derived from aspartyl residues in affinity-purified calmodulin. The role of conformational flexibility in spontaneous isoaspartyl formation. , 1989, Journal of Biological Chemistry.

[14]  S. Clarke,et al.  Succinimide formation from aspartyl and asparaginyl peptides as a model for the spontaneous degradation of proteins. , 1989, The Journal of biological chemistry.

[15]  D. Aswad,et al.  Fragmentation of isoaspartyl peptides and proteins by carboxypeptidase Y: release of isoaspartyl dipeptides as a result of internal and external cleavage. , 1990, Biochemistry.

[16]  S. Clarke,et al.  Structural elements affecting the recognition of L-isoaspartyl residues by the L-isoaspartyl/D-aspartyl protein methyltransferase. Implications for the repair hypothesis. , 1991, The Journal of biological chemistry.

[17]  S. Clarke,et al.  Recognition of D-aspartyl residues in polypeptides by the erythrocyte L-isoaspartyl/D-aspartyl protein methyltransferase. Implications for the repair hypothesis. , 1992, The Journal of biological chemistry.

[18]  D. Selkoe,et al.  Mass spectrometry of purified amyloid beta protein in Alzheimer's disease. , 1992, The Journal of biological chemistry.

[19]  Khadija Iqbal,et al.  Peptide compositions of the cerebrovascular and senile plaque core amyloid deposits of Alzheimer's disease. , 1993, Archives of biochemistry and biophysics.

[20]  L. Petrucelli,et al.  Improved method for hydrolyzing proteins and peptides without inducing racemization and for determining their true D-amino acid content. , 1993, Analytical biochemistry.

[21]  M J Ball,et al.  Structural alterations in the peptide backbone of beta-amyloid core protein may account for its deposition and stability in Alzheimer's disease. , 1993, The Journal of biological chemistry.

[22]  K. Harada,et al.  Simultaneous racemization and isomerization at specific aspartic acid residues in alpha B-crystallin from the aged human lens. , 1994, Biochimica et biophysica acta.

[23]  D. Selkoe,et al.  Normal and abnormal biology of the beta-amyloid precursor protein. , 1994, Annual review of neuroscience.

[24]  S. Clarke,et al.  Repair of spontaneously deamidated HPr phosphocarrier protein catalyzed by the L-isoaspartate-(D-aspartate) O-methyltransferase. , 1994, The Journal of biological chemistry.

[25]  T. Shirasawa,et al.  Racemization of Asp23 residue affects the aggregation properties of Alzheimer amyloid beta protein analogues. , 1994, The Journal of biological chemistry.

[26]  S. Clarke,et al.  Expression and purification of a human recombinant methyltransferase that repairs damaged proteins. , 1995, Protein expression and purification.

[27]  D. Mann,et al.  Dominant and differential deposition of distinct β-amyloid peptide species, Aβ N3(pE), in senile plaques , 1995, Neuron.

[28]  L K Duffy,et al.  Stabilization of secondary structure of Alzheimer beta-protein by aluminum(III) ions and D-Asp substitutions. , 1995, Biochemical and biophysical research communications.

[29]  I. Kaneko,et al.  Suppression of Mitochondrial Succinate Dehydrogenase, a Primary Target of β‐Amyloid, and Its Derivative Racemized at Ser Residue , 1995, Journal of neurochemistry.

[30]  D. Aswad,et al.  Molecular aging of tubulin: accumulation of isoaspartyl sites in vitro and in vivo. , 1996, Biochemistry.

[31]  Hendrik Zipse,et al.  ACCELERATED RACEMIZATION OF ASPARTIC ACID AND ASPARAGINE RESIDUES VIA SUCCINIMIDE INTERMEDIATES : AN AB INITIO THEORETICAL EXPLORATION OF MECHANISM , 1996 .

[32]  M. Emmerling,et al.  Isolation, chemical characterization, and quantitation of A beta 3-pyroglutamyl peptide from neuritic plaques and vascular amyloid deposits. , 1997, Biochemical and biophysical research communications.

[33]  M. Emmerling,et al.  Irreversible dimerization/tetramerization and post-translational modifications inhibit proteolytic degradation of A beta peptides of Alzheimer's disease. , 1998, Biochimica et biophysica acta.