Superoxide dismutase in familial amyotrophic lateral sclerosis: Models for gain of function

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[43] YAMA/CPP32-BETA, A MAMMALIAN HOMOLOG OF CED-3, IS A CRMA-INHIBITABLE PROTEASE THAT CLEAVES THE DEATH SUBSTRATE POLY(ADP-RIBOSE) POLYMERASE [J]. CELL, 1995, 81 (05) : 801 - 809

[44] DOWN-REGULATION OF COPPER/ZINC SUPEROXIDE-DISMUTASE CAUSES APOPTOTIC DEATH IN PC12 NEURONAL CELLS [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (14) : 6384 - 6387

[45] WEISS JH, 1993, NEURON, V10, P43, DOI 10.1016/0896-6273(93)90240-R

[46] AN ADVERSE PROPERTY OF A FAMILIAL ALS-LINKED SOD1 MUTATION CAUSES MOTOR-NEURON DISEASE CHARACTERIZED BY VACUOLAR DEGENERATION OF MITOCHONDRIA [J]. NEURON, 1995, 14 (06) : 1105 - 1116

[47] YIM MB, 1993, J BIOL CHEM, V268, P4099

[48] THE C-ELEGANS CELL-DEATH GENE CED-3 ENCODES A PROTEIN SIMILAR TO MAMMALIAN INTERLEUKIN-1-BETA-CONVERTING ENZYME [J]. CELL, 1993, 75 (04) : 641 - 652

[41] AMYOTROPHIC LATERAL SCLEROSIS .2. ETIOPATHOGENESIS [J]. ANNALS OF NEUROLOGY, 1985, 18 (04) : 419 - 431

[42] AMYOTROPHIC LATERAL SCLEROSIS .1. CLINICAL-FEATURES, PATHOLOGY, AND ETHICAL ISSUES IN MANAGEMENT [J]. ANNALS OF NEUROLOGY, 1985, 18 (03) : 271 - 280

[43] YAMA/CPP32-BETA, A MAMMALIAN HOMOLOG OF CED-3, IS A CRMA-INHIBITABLE PROTEASE THAT CLEAVES THE DEATH SUBSTRATE POLY(ADP-RIBOSE) POLYMERASE [J]. CELL, 1995, 81 (05) : 801 - 809

[44] DOWN-REGULATION OF COPPER/ZINC SUPEROXIDE-DISMUTASE CAUSES APOPTOTIC DEATH IN PC12 NEURONAL CELLS [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (14) : 6384 - 6387

[45] WEISS JH, 1993, NEURON, V10, P43, DOI 10.1016/0896-6273(93)90240-R

[46] AN ADVERSE PROPERTY OF A FAMILIAL ALS-LINKED SOD1 MUTATION CAUSES MOTOR-NEURON DISEASE CHARACTERIZED BY VACUOLAR DEGENERATION OF MITOCHONDRIA [J]. NEURON, 1995, 14 (06) : 1105 - 1116

[47] YIM MB, 1993, J BIOL CHEM, V268, P4099

[48] THE C-ELEGANS CELL-DEATH GENE CED-3 ENCODES A PROTEIN SIMILAR TO MAMMALIAN INTERLEUKIN-1-BETA-CONVERTING ENZYME [J]. CELL, 1993, 75 (04) : 641 - 652