Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Steve Keve"'
Autor:
Mark T. Butt, Robert B. Boyd, Steve Keve, Brian R. Vuillemenot, Donald G. Musson, Rhea Cahayag, Randall P. Reed, Charles A. O'Neill, Derek Kennedy, Laurie S. Tsuruda
Publikováno v:
Toxicology and Applied Pharmacology. 277:49-57
CLN2 disease is caused by deficiency in tripeptidyl peptidase-1 (TPP1), leading to neurodegeneration and death. The safety, pharmacokinetics (PK), and CNS distribution of recombinant human TPP1 (rhTPP1) were characterized following a single intracere
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f833c2194ddcd5445f8772d28bde3c49
https://doi.org/10.1016/j.taap.2014.03.005
https://doi.org/10.1016/j.taap.2014.03.005
Autor:
Laurie S. Tsuruda, Steve Keve, Derek Kennedy, Istvan Sohar, Su Xu, Eugen Koren, Martin L. Katz, Rhea Cahayag, Shinichi Kanazono, Pascale M.N. Tiger, Peter Lobel, Stuart Bunting, Joan R. Coates, Brian R. Vuillemenot, Charles A. O'Neill
Publikováno v:
Molecular Genetics and Metabolism. 104:325-337
Late infantile neuronal ceroid lipofuscinosis (LINCL) is caused by mutations in the gene encoding tripeptidyl-peptidase 1 (TPP1). LINCL patients accumulate lysosomal storage materials in the CNS accompanied by neurodegeneration, blindness, and functi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ddda46625ced3a3cc77f4865f20c399d
https://doi.org/10.1016/j.ymgme.2011.06.018
https://doi.org/10.1016/j.ymgme.2011.06.018
Autor:
Martin L. Katz, Eric L. Adams, Mark T. Butt, Joshua Henshaw, Steve Keve, Joan R. Coates, Donald G. Musson, Derek Kennedy, Jonathan D. Cooper, Thom Doeleman, Sarmi Sri, Brian R. Vuillemenot, Randall P. Reed, Gayle C. Johnson, Rhea Cahayag, Charles A. O'Neill, Laurie S. Tsuruda, Andrew Wong
Publikováno v:
Molecular genetics and metabolism. 114(2)
The CLN2 form of neuronal ceroid lipofuscinosis, a type of Batten disease, is a lysosomal storage disorder caused by a deficiency of the enzyme tripeptidyl peptidase-1 (TPP1). Patients exhibit progressive neurodegeneration and loss of motor, cognitiv
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::305cd0a5b13658f1d3aba7b45a2895d2
https://pubmed.ncbi.nlm.nih.gov/25257657
https://pubmed.ncbi.nlm.nih.gov/25257657
Publikováno v:
Clinical Immunology and Immunopathology. 59:246-255
Myasthenia gravis (MG) is an autoimmune neuromuscular disease, characterized by muscle weakness and electrophysiological abnormality. No treatment which would reliably induce permanent clinical remission of MG is yet available. The therapeutic effica
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5a23f3c5c372a94545c95be432714ae5
https://doi.org/10.1016/0090-1229(91)90022-3
https://doi.org/10.1016/0090-1229(91)90022-3
Publikováno v:
Clinical immunology and immunopathology. 62(2)
The I-A beta gene has been implicated in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG), with amino acids at positions 67, 70, and 71 of the I-A beta b chain that play a crucial role. In addition, the cell surface expression of
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::88f9cca32f44a688ecf36d844853fb3a
https://pubmed.ncbi.nlm.nih.gov/1730162
https://pubmed.ncbi.nlm.nih.gov/1730162
Publikováno v:
Immunogenetics. 31(4)
Mice bearing the H-2 bhaplotype are susceptible to the development of experimental autoimmune myasthenia gravis (EAMG), induced by acetylcholine receptor (AChR) autoimmunity. One of the genes influencing EAMG susceptibility has been mapped to the A b
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::382af1462cedf9c3c7fe30bc9ea3acd8
https://pubmed.ncbi.nlm.nih.gov/2109730
https://pubmed.ncbi.nlm.nih.gov/2109730
Publikováno v:
Clinical Immunology and Immunopathology. 60:495
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1a725ef3fc401be7504f9e5bd3157183
https://doi.org/10.1016/0090-1229(91)90104-i
https://doi.org/10.1016/0090-1229(91)90104-i