The absence of mitochondrial thioredoxin 2 causes massive apoptosis, exencephaly, and early embryonic lethality in homozygous mice

Molecular and Cellular Biology

Volumn 23, Issue 3, 2003, Pages 916-922

  Nonn, Larisa ^a   Williams, Ryan R ^a   Erickson, Robert P ^a   Powis, Garth ^a  

^a UNIVERSITY OF ARIZONA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIOXIDANT; PROTEIN; PROTEIN TRX2; SIGNAL PEPTIDE; SUPEROXIDE DISMUTASE; THIOREDOXIN; THIOREDOXIN 2; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL RESPIRATION; CELL VIABILITY; CONTROLLED STUDY; EMBRYO; EMBRYO DEATH; EMBRYO DEVELOPMENT; EXENCEPHALY; GENE INSERTION; GENE MUTATION; GENE SILENCING; GENOTYPE; MITOCHONDRION; MOUSE; NEURAL TUBE; NEURAL TUBE DEFECT; NIDATION; NONHUMAN; OXIDATION REDUCTION STATE; OXIDATIVE PHOSPHORYLATION; PHENOTYPE; PRIORITY JOURNAL; PROTEIN DEFECT; PROTEIN EXPRESSION; REGULATORY MECHANISM;

ANIMALS; APOPTOSIS; FEMALE; FETAL DEATH; GESTATIONAL AGE; HETEROZYGOTE; HOMOZYGOTE; MEMBRANE PROTEINS; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MITOCHONDRIA; NEURAL TUBE DEFECTS; PHENOTYPE; PREGNANCY; RNA, MESSENGER; THIOREDOXIN;

ANIMALIA; MAMMALIA;

EID: 0037305881     PISSN: 02707306     EISSN: None     Source Type: Journal    
DOI: 10.1128/MCB.23.3.916-922.2003     Document Type: Article

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