M. Lee

发表

Neurofilament subunit NF-H modulates axonal diameter by selectively slowing neurofilament transport

T. Crawford, D. Cleveland, J. Marszalek, 1996, The Journal of cell biology.

ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions

D. Borchelt, D. Price, L. Bruijn, 1997, Neuron.

Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity.

D. Borchelt, D. Price, P. Wong, 1994, Proceedings of the National Academy of Sciences of the United States of America.

Mutations associated with amyotrophic lateral sclerosis convert superoxide dismutase from an antiapoptotic gene to a proapoptotic gene: studies in yeast and neural cells.

D. Borchelt, P. Wong, R. Gwinn, 1995, Proceedings of the National Academy of Sciences of the United States of America.

Superoxide Dismutase 1 Subunits with Mutations Linked to Familial Amyotrophic Lateral Sclerosis Do Not Affect Wild-type Subunit Function (*)

D. Borchelt, D. Price, P. Wong, 1995, The Journal of Biological Chemistry.

Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model.

D. Borchelt, C. Ross, N. Jenkins, 2010, Human molecular genetics.

Identification and characterization of a mouse homologue of the spinal muscular atrophy-determining gene, survival motor neuron.

D. Price, A. Bergin, S. Sisodia, 1997, Gene.

Motor neuron disease and model systems: aetiologies, mechanisms and therapies.

D. Borchelt, D. Price, P. Wong, 1996, Ciba Foundation symposium.

Amyotrophic lateral sclerosis and Alzheimer disease. Lessons from model systems.

D. Borchelt, D. Price, P. Wong, 1997, Revue neurologique.

Neurofilaments, radial growth of axons, and mechanisms of motor neuron disease.

L. Bruijn, D. Cleveland, J. Marszalek, 1996, Cold Spring Harbor symposia on quantitative biology.

Neurodegenerative diseases and model systems.

D. Borchelt, D. Price, P. Wong, 1996, Cold Spring Harbor symposia on quantitative biology.

Neurofilaments are obligate heteropolymers in vivo

P. Wong, D. Cleveland, Michael K. Lee, 1993, The Journal of cell biology.

Assessment of normal and mutant human presenilin function in Caenorhabditis elegans.

I. Greenwald, S. Sisodia, Michael K. Lee, 1996, Proceedings of the National Academy of Sciences of the United States of America.

Familial amyotrophic lateral sclerosis and Alzheimer's disease. Transgenic models.

D. Borchelt, D. Price, P. Wong, 1998, Advances in experimental medicine and biology.

Mechanisms of selective motor neuron death in transgenic mouse models of motor neuron disease

D. Borchelt, D. Price, P. Wong, 1996, Neurology.

Neurofilament function and dysfunction: involvement in axonal growth and neuronal disease.

D. Cleveland, M. Lee, 1994, Current opinion in cell biology.

Subunit composition of neurofilaments specifies axonal diameter

T. Crawford, P. Wong, S. Hsieh, 1996, The Journal of cell biology.

A vector for expressing foreign genes in the brains and hearts of transgenic mice.

D L Price, D. Borchelt, D. Price, 1996, Genetic analysis : biomolecular engineering.

Neuronal intermediate filaments.

D. Cleveland, Michael K. Lee, D W Cleveland, 1996, Annual review of neuroscience.

Neurodegenerative phenotypes in an A 53 T a-synuclein transgenic mouse model are independent of LRRK 2

A. Goris, W. Robberecht, H. J. Schelhaas, 2012 .

Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo.

D. Yager, S. Sisodia, C. Prada, 1996, Neuron.