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C M Knudson

Showing results (21-30 of 42) with videos related to

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Nature Medicine|November 14, 1997
Apoptosis-associated signaling pathways are required for chemotherapy-mediated female germ cell destructionG I Perez, C M Knudson, L Leykin, et al.
Science (New York, N.Y.)|October 6, 1995
Bax-deficient mice with lymphoid hyperplasia and male germ cell deathC M Knudson, K S Tung, W G Tourtellotte, et al.
Annals of the New York Academy of Sciences|January 1, 1989
Role of the ryanodine receptor of skeletal muscle in excitation-contraction couplingM Fill, J J Ma, C M Knudson, et al.
Nature Medicine|December 10, 1998
Hyperglycemia induces apoptosis in pre-implantation embryos through cell death effector pathwaysK H Moley, M M Chi, C M Knudson, et al.
The Journal of Biological Chemistry|June 15, 1993
Primary structure and topological analysis of a skeletal muscle-specific junctional sarcoplasmic reticulum glycoprotein (triadin)C M Knudson, K K Stang, C R Moomaw, et al.
Experimental Neurology|July 31, 1998
Placement of the BCL2 family member BAX in the death pathway of sympathetic neurons activated by trophic factor deprivationT L Deckwerth, R M Easton, C M Knudson, et al.
Proceedings of the National Academy of Sciences of the United States of America|March 18, 1997
bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosisM E McCurrach, T M Connor, C M Knudson, et al.
The Journal of Biological Chemistry|June 15, 1988
Evidence for the association of dystrophin with the transverse tubular system in skeletal muscleC M Knudson, E P Hoffman, S D Kahl, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|March 14, 1998
Bax involvement in p53-mediated neuronal cell deathH Xiang, Y Kinoshita, C M Knudson, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|March 14, 1998
Widespread elimination of naturally occurring neuronal death in Bax-deficient miceF A White, C R Keller-Peck, C M Knudson, et al.
Pageof 5

Showing results (21-30 of 42) with videos related to

Sort By:
Pageof 5
Nature Medicine|November 14, 1997
Apoptosis-associated signaling pathways are required for chemotherapy-mediated female germ cell destructionG I Perez, C M Knudson, L Leykin, et al.
Science (New York, N.Y.)|October 6, 1995
Bax-deficient mice with lymphoid hyperplasia and male germ cell deathC M Knudson, K S Tung, W G Tourtellotte, et al.
Annals of the New York Academy of Sciences|January 1, 1989
Role of the ryanodine receptor of skeletal muscle in excitation-contraction couplingM Fill, J J Ma, C M Knudson, et al.
Nature Medicine|December 10, 1998
Hyperglycemia induces apoptosis in pre-implantation embryos through cell death effector pathwaysK H Moley, M M Chi, C M Knudson, et al.
The Journal of Biological Chemistry|June 15, 1993
Primary structure and topological analysis of a skeletal muscle-specific junctional sarcoplasmic reticulum glycoprotein (triadin)C M Knudson, K K Stang, C R Moomaw, et al.
Experimental Neurology|July 31, 1998
Placement of the BCL2 family member BAX in the death pathway of sympathetic neurons activated by trophic factor deprivationT L Deckwerth, R M Easton, C M Knudson, et al.
Proceedings of the National Academy of Sciences of the United States of America|March 18, 1997
bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosisM E McCurrach, T M Connor, C M Knudson, et al.
The Journal of Biological Chemistry|June 15, 1988
Evidence for the association of dystrophin with the transverse tubular system in skeletal muscleC M Knudson, E P Hoffman, S D Kahl, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|March 14, 1998
Bax involvement in p53-mediated neuronal cell deathH Xiang, Y Kinoshita, C M Knudson, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|March 14, 1998
Widespread elimination of naturally occurring neuronal death in Bax-deficient miceF A White, C R Keller-Peck, C M Knudson, et al.
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