Molecular mechanisms of fibrillogenesis and the protective role of amyloid P component: two possible avenues for therapy.
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S. Radford | D. Booth | C. Robinson | L. Serpell | C. Blake | P. Fraser | L. Lovat | M. Sunde | M. Pepys | P. Hawkins | G. Tennent | A. Soutar | J. Campistol | M. Persey | V. Bellotti | W. Hutchinson | S. Tan | S. Booth | S. Madhoo | R. van Zyl-Smit | W. Hutchinson | G. Tennent | J. M. Campistol | P. E. Fraser | L. Lovat | D. R. Booth | S. Tan | A. K. Soutart | P. Hawkins | S. E. Radford | C. V. Robinson | L. Serpell | C. C. F. Blake
[1] D. Booth,et al. A new apolipoprotein Al variant, Trp50Arg, causes hereditary amyloidosis. , 1995, QJM : monthly journal of the Association of Physicians.
[2] J. Hofrichter,et al. Kinetics and mechanism of deoxyhemoglobin S gelation: a new approach to understanding sickle cell disease. , 1974, Proceedings of the National Academy of Sciences of the United States of America.
[3] M. Pepys,et al. Isolation of C-reactive protein by affinity chromatography. , 1977, Clinical and experimental immunology.
[4] S. Younkin,et al. Serum Amyloid P in Alzheimer's Disease , 1991, Annals of the New York Academy of Sciences.
[5] A. Cohen,et al. Redistribution of amyloid deposits. , 1980, The American journal of pathology.
[6] B. Frangione,et al. Ten to fourteen residue peptides of Alzheimer's disease protein are sufficient for amyloid fibril formation and its characteristic x-ray diffraction pattern. , 1987, Biochemical and biophysical research communications.
[7] B. Wallin,et al. Clinical improvement and amyloid regression after liver transplantation in hereditary transthyretin amyloidosis , 1993, The Lancet.
[8] A. Feinstein,et al. Calcium-dependent aggregation of human serum amyloid P component. , 1982, Biochimica et biophysica acta.
[9] H. Merkle,et al. Interfacial adsorption and aggregation associated changes in secondary structure of human calcitonin monitored by ATR-FTIR spectroscopy. , 1994, Biochemistry.
[10] D. Booth,et al. Human lysozyme gene mutations cause hereditary systemic amyloidosis , 1993, Nature.
[11] P. Hawkins. Studies with radiolabelled serum amyloid P component provide evidence for turnover and regression of amyloid deposits in vivo. , 1994, Clinical science.
[12] Amyloid P-Component: Structure and Properties , 1986 .
[13] Robin W. Briehl,et al. Nucleation and growth of fibres and gel formation in sickle cell haemoglobin , 1990, Nature.
[14] U Aebi,et al. Architecture and polymorphism of fibrillar supramolecular assemblies produced by in vitro aggregation of human calcitonin. , 1995, Journal of structural biology.
[15] A. Drake,et al. The structure and mechanism of formation of human calcitonin fibrils. , 1993, The Journal of biological chemistry.
[16] D. Parry,et al. α‐Helical coiled coils and bundles: How to design an α‐helical protein , 1990 .
[17] K. Sletten,et al. Massive Vascular AA‐Amyloidosis: A Histologically and Biochemically Distinctive Subtype of Reactive Systemic Amyloidosis , 1989, Scandinavian journal of immunology.
[18] M. Pepys,et al. The pentraxins, C-reactive protein and serum amyloid P component, are cleared and catabolized by hepatocytes in vivo. , 1994, The Journal of clinical investigation.
[19] F. Tashiro,et al. Role of serum amyloid P component for systemic amyloidosis in transgenic mice carrying human mutant transthyretin gene. , 1991, Gerontology.
[20] C. Betsholtz,et al. Islet amyloid polypeptide: pinpointing amino acid residues linked to amyloid fibril formation. , 1990, Proceedings of the National Academy of Sciences of the United States of America.
[21] M. Pepys,et al. Metabolic studies of radioiodinated serum amyloid P component in normal subjects and patients with systemic amyloidosis. , 1990, The Journal of clinical investigation.
[22] Maria João,et al. Transthyretin mutations in health and disease , 1995, Human mutation.
[23] M. Pepys,et al. Human serum amyloid P component, a circulating lectin with specificity for the cyclic 4,6-pyruvate acetal of galactose. Interactions with various bacteria. , 1985, The Biochemical journal.
[24] J. Hardy. Framing β–amyloid , 1992, Nature Genetics.
[25] S. Wimalawansa. Effects of in vivo stimulation on molecular forms of circulatory calcitonin and calcitonin gene-related peptide in man , 1990, Molecular and Cellular Endocrinology.
[26] M. Pepys,et al. Binding specificity of serum amyloid P component for the pyruvate acetal of galactose , 1984, The Journal of experimental medicine.
[27] R. Kisilevsky,et al. Sulfated glycosaminoglycans: a common constituent of all amyloids? , 1987, Laboratory investigation; a journal of technical methods and pathology.
[28] A. Scheibel,et al. Microtubule-associated proteins tau and amyloid P component in Alzheimer's disease , 1993, Brain Research.
[29] T. Rademacher,et al. Human serum amyloid P component is an invariant constituent of amyloid deposits and has a uniquely homogeneous glycostructure. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[30] P. Westermark,et al. The N-terminal segment of protein AA determines its fibrillogenic property. , 1992, Biochemical and biophysical research communications.
[31] A. King,et al. Scintigraphic quantification and serial monitoring of human visceral amyloid deposits provide evidence for turnover and regression. , 1993, The Quarterly journal of medicine.
[32] J. Hofrichter,et al. Kinetic studies on photolysis-induced gelation of sickle cell hemoglobin suggest a new mechanism. , 1980, Biophysical journal.
[33] D. Booth,et al. Hereditary hepatic and systemic amyloidosis caused by a new deletion/insertion mutation in the apolipoprotein AI gene. , 1996, The Journal of clinical investigation.
[34] P. Lansbury,et al. A chemical approach to elucidate tin mechanism of transthyretin and β-protein amyloid fibril formation , 1994 .
[35] T. Wisniewski,et al. Conformational mimicry in Alzheimer's disease. Role of apolipoproteins in amyloidogenesis. , 1995, The American journal of pathology.
[36] J. Hofrichter,et al. Kinetics of sickle hemoglobin polymerization. II. A double nucleation mechanism. , 1985, Journal of molecular biology.
[37] H. Chui,et al. Localization of amyloid P component in human brain: Vascular staining patterns and association with alzheimer's disease lesions , 1995, The Journal of comparative neurology.
[38] Robert S. Huckman,et al. A protease‐sensitive site in the proposed Ca2+‐binding region of human serum amyloid P component and other pentraxins , 1992, Protein science : a publication of the Protein Society.
[39] P. Westermark,et al. Normal transthyretin and synthetic transthyretin fragments form amyloid-like fibrils in vitro. , 1991, Biochemical and biophysical research communications.
[40] J. Coe,et al. Amyloidosis and female protein in the Syrian hamster. Concurrent regulation by sex hormones , 1990, The Journal of experimental medicine.
[41] F. Tashiro,et al. Effect of serum amyloid P component level on transthyretin-derived amyloid deposition in a transgenic mouse model of familial amyloidotic polyneuropathy. , 1992, The American journal of pathology.
[42] P. Lansbury,et al. The carboxy terminus of the beta amyloid protein is critical for the seeding of amyloid formation: implications for the pathogenesis of Alzheimer's disease. , 1993, Biochemistry.
[43] R. Kalaria,et al. Widespread serum amyloid P immunoreactivity in cortical amyloid deposits and the neurofibrillary pathology of Alzheimer's disease and other degenerative disorders , 1991, Neuropathology and applied neurobiology.
[44] T. Blundell,et al. Structure of pentameric human serum amyloid P component , 1994, Nature.
[45] D. W. Hayden,et al. Pulmonary vascular amyloidosis in aged dogs. A new form of spontaneously occurring amyloidosis derived from apolipoprotein AI. , 1992, The American journal of pathology.
[46] M. Pepys,et al. DIAGNOSTIC RADIONUCLIDE IMAGING OF AMYLOID: BIOLOGICAL TARGETING BY CIRCULATING HUMAN SERUM AMYLOID P COMPONENT , 1988, The Lancet.
[47] M. Pepys,et al. Isolation and characterization of the integral glycosaminoglycan constituents of human amyloid A and monoclonal light-chain amyloid fibrils. , 1991, The Biochemical journal.
[48] P. Lansbury,et al. Seeding “one-dimensional crystallization” of amyloid: A pathogenic mechanism in Alzheimer's disease and scrapie? , 1993, Cell.
[49] M. Pepys,et al. Evaluation of systemic amyloidosis by scintigraphy with 123I-labeled serum amyloid P component. , 1990, The New England journal of medicine.
[50] P. Butler,et al. Pentraxin-chromatin interactions: serum amyloid P component specifically displaces H1-type histones and solubilizes native long chromatin , 1990, The Journal of experimental medicine.
[51] R. Kalaria,et al. Serum amyloid P immunoreactivity in hippocampal tangles, plaques and vessels: implications for leakage across the blood-brain barrier in Alzheimer's disease , 1990, Brain Research.
[52] M. Pepys,et al. Imaging of haemodialysis-associated amyloidosis with 123I-serum amyloid P component , 1991, The Lancet.
[53] Brian J Cummings,et al. Image analysis of β-amyloid load in Alzheimer's disease and relation to dementia severity , 1995, The Lancet.
[54] P. Woo,et al. Serum amyloid P component scintigraphy and turnover studies for diagnosis and quantitative monitoring of AA amyloidosis in juvenile rheumatoid arthritis. , 1993, Arthritis and rheumatism.
[55] G. Perry,et al. Amyloid P component and other acute-phase proteins associated with cerebellar Aβ-deposits in Alzheimer's disease , 1993, Brain Research.
[56] C. Maury,et al. Amyloid fibril formation in gelsolin-derived amyloidosis. Definition of the amyloidogenic region and evidence of accelerated amyloid formation of mutant Asn-187 and Tyr-187 gelsolin peptides. , 1994, Laboratory investigation; a journal of technical methods and pathology.
[57] M. Pepys,et al. SPECIFIC CHEMICAL DISSOCIATION OF FIBRILLAR AND NON-FIBRILLAR COMPONENTS OF AMYLOID DEPOSITS , 1984, The Lancet.
[58] M. Pepys,et al. Experimental amyloidosis in the hamster: correlation between hamster female protein levels and amyloid deposition. , 1989, Clinical and experimental immunology.
[59] L. Lovat,et al. Serum amyloid P component prevents proteolysis of the amyloid fibrils of Alzheimer disease and systemic amyloidosis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[60] K. Kanaori,et al. Study of human calcitonin fibrillation by proton nuclear magnetic resonance spectroscopy. , 1995, Biochemistry.
[61] K. Sletten,et al. Apolipoprotein A1-derived amyloid in human aortic atherosclerotic plaques. , 1995, The American journal of pathology.
[62] L. Pinteric,et al. THE STRUCTURE AND BINDING CHARACTERISTICS OF SERUM AMYLOID PROTEIN (9.5S α1‐glycoprotein) , 1982 .
[63] P. Butler,et al. Serum amyloid P component is the major calcium-dependent specific DNA binding protein of the serum. , 1987, Biochemical and biophysical research communications.
[64] R. Kyle,et al. Nomenclature and classification of amyloid and amyloidoses , 1992, Journal of internal medicine.