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W Cleveland

Showing results (391-400 of 499) with videos related to

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Molecular Therapy. Nucleic Acids|April 25, 2023
GOLGA8 increases bulk antisense oligonucleotide uptake and activity in mammalian cellsMoira A McMahon, Meghdad Rahdar, Swagatam Mukhopadhyay, et al.
Nature Cell Biology|June 5, 2019
DNA replication acts as an error correction mechanism to maintain centromere identity by restricting CENP-A to centromeresYael Nechemia-Arbely, Karen H Miga, Ofer Shoshani, et al.
Molecular Therapy : the Journal of the American Society of Gene Therapy|September 7, 2013
Therapeutic AAV9-mediated suppression of mutant SOD1 slows disease progression and extends survival in models of inherited ALSKevin D Foust, Desirée L Salazar, Shibi Likhite, et al.
Plos One|August 7, 2008
Messenger RNA oxidation occurs early in disease pathogenesis and promotes motor neuron degeneration in ALSYueming Chang, Qiongman Kong, Xiu Shan, 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.
Plos One|August 24, 2012
Human neural stem cell replacement therapy for amyotrophic lateral sclerosis by spinal transplantationMichael P Hefferan, Jan Galik, Osamu Kakinohana, et al.
Clinical Pediatrics|May 1, 1990
Height screening in the community. The commercialization of growth. The role of the pediatricianA L Rosenbloom, C Alves, W W Cleveland, et al.
Cell|September 4, 2012
Single-stranded RNAs use RNAi to potently and allele-selectively inhibit mutant huntingtin expressionDongbo Yu, Hannah Pendergraff, Jing Liu, 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.
Pageof 50

Showing results (391-400 of 499) with videos related to

Sort By:
Pageof 50
Molecular Therapy. Nucleic Acids|April 25, 2023
GOLGA8 increases bulk antisense oligonucleotide uptake and activity in mammalian cellsMoira A McMahon, Meghdad Rahdar, Swagatam Mukhopadhyay, et al.
Nature Cell Biology|June 5, 2019
DNA replication acts as an error correction mechanism to maintain centromere identity by restricting CENP-A to centromeresYael Nechemia-Arbely, Karen H Miga, Ofer Shoshani, et al.
Molecular Therapy : the Journal of the American Society of Gene Therapy|September 7, 2013
Therapeutic AAV9-mediated suppression of mutant SOD1 slows disease progression and extends survival in models of inherited ALSKevin D Foust, Desirée L Salazar, Shibi Likhite, et al.
Plos One|August 7, 2008
Messenger RNA oxidation occurs early in disease pathogenesis and promotes motor neuron degeneration in ALSYueming Chang, Qiongman Kong, Xiu Shan, 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.
Plos One|August 24, 2012
Human neural stem cell replacement therapy for amyotrophic lateral sclerosis by spinal transplantationMichael P Hefferan, Jan Galik, Osamu Kakinohana, et al.
Clinical Pediatrics|May 1, 1990
Height screening in the community. The commercialization of growth. The role of the pediatricianA L Rosenbloom, C Alves, W W Cleveland, et al.
Cell|September 4, 2012
Single-stranded RNAs use RNAi to potently and allele-selectively inhibit mutant huntingtin expressionDongbo Yu, Hannah Pendergraff, Jing Liu, 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.
Pageof 50