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D W Cleveland

Showing results (161-170 of 174) with videos related to

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The Journal of Cell Biology|April 1, 1987
Molecular cloning of cDNA for CENP-B, the major human centromere autoantigenW C Earnshaw, K F Sullivan, P S Machlin, et al.
Science (New York, N.Y.)|September 22, 1998
Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1L I Bruijn, M K Houseweart, S Kato, et al.
Acta Neuropathologica|October 25, 2000
Advanced glycation endproduct-modified superoxide dismutase-1 (SOD1)-positive inclusions are common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutations and transgenic mice expressing human SOD1 with a G85R mutationS Kato, S Horiuchi, J Liu, et al.
The Journal of Cell Biology|June 1, 1996
Subunit composition of neurofilaments specifies axonal diameterZ Xu, J R Marszalek, M K Lee, et al.
The Journal of Biological Chemistry|February 17, 1995
Superoxide dismutase 1 subunits with mutations linked to familial amyotrophic lateral sclerosis do not affect wild-type subunit functionD R Borchelt, M Guarnieri, P C Wong, et al.
Neuron|June 1, 1995
An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondriaP C Wong, C A Pardo, D R Borchelt, et al.
Neuropathology : Official Journal of the Japanese Society of Neuropathology|April 17, 2001
Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutationS Kato, K Nakashima, S Horiuchi, et al.
Proceedings of the National Academy of Sciences of the United States of America|August 16, 1994
Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activityD R Borchelt, M K Lee, H S Slunt, et al.
Neurology|October 1, 1996
Mechanisms of selective motor neuron death in transgenic mouse models of motor neuron diseaseD W Cleveland, L I Bruijn, P C Wong, et al.
Ciba Foundation Symposium|January 1, 1996
Motor neuron disease and model systems: aetiologies, mechanisms and therapiesD L Price, V E Koliatsos, P C Wong, et al.
Pageof 18

Showing results (161-170 of 174) with videos related to

Sort By:
Pageof 18
The Journal of Cell Biology|April 1, 1987
Molecular cloning of cDNA for CENP-B, the major human centromere autoantigenW C Earnshaw, K F Sullivan, P S Machlin, et al.
Science (New York, N.Y.)|September 22, 1998
Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1L I Bruijn, M K Houseweart, S Kato, et al.
Acta Neuropathologica|October 25, 2000
Advanced glycation endproduct-modified superoxide dismutase-1 (SOD1)-positive inclusions are common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutations and transgenic mice expressing human SOD1 with a G85R mutationS Kato, S Horiuchi, J Liu, et al.
The Journal of Cell Biology|June 1, 1996
Subunit composition of neurofilaments specifies axonal diameterZ Xu, J R Marszalek, M K Lee, et al.
The Journal of Biological Chemistry|February 17, 1995
Superoxide dismutase 1 subunits with mutations linked to familial amyotrophic lateral sclerosis do not affect wild-type subunit functionD R Borchelt, M Guarnieri, P C Wong, et al.
Neuron|June 1, 1995
An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondriaP C Wong, C A Pardo, D R Borchelt, et al.
Neuropathology : Official Journal of the Japanese Society of Neuropathology|April 17, 2001
Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutationS Kato, K Nakashima, S Horiuchi, et al.
Proceedings of the National Academy of Sciences of the United States of America|August 16, 1994
Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activityD R Borchelt, M K Lee, H S Slunt, et al.
Neurology|October 1, 1996
Mechanisms of selective motor neuron death in transgenic mouse models of motor neuron diseaseD W Cleveland, L I Bruijn, P C Wong, et al.
Ciba Foundation Symposium|January 1, 1996
Motor neuron disease and model systems: aetiologies, mechanisms and therapiesD L Price, V E Koliatsos, P C Wong, et al.
Pageof 18