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Volumn 16, Issue 1, 2000, Pages 109-117
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Nitric oxide-mediated apoptosis in human breast cancer cells requires changes in mitochondrial functions and is independent of CD95 (APO-1/Fas).
a
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Author keywords
[No Author keywords available]
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Indexed keywords
BAX PROTEIN, HUMAN;
CARRIER PROTEIN;
CASPASE;
CYTOCHROME C;
FAS ANTIGEN;
FAS LIGAND;
FASLG PROTEIN, HUMAN;
MEMBRANE PROTEIN;
MESSENGER RNA;
NITRIC OXIDE;
ONCOPROTEIN;
PROTEIN BAX;
PROTEIN BCL 2;
PROTEIN TYROSINE PHOSPHATASE;
PTPN13 PROTEIN, HUMAN;
REACTIVE OXYGEN METABOLITE;
APOPTOSIS;
ARTICLE;
BIOSYNTHESIS;
BREAST TUMOR;
CELL CULTURE;
CELL MEMBRANE POTENTIAL;
DRUG EFFECT;
ENZYME ACTIVATION;
ENZYMOLOGY;
HUMAN;
METABOLISM;
MITOCHONDRION;
PHYSIOLOGY;
UPREGULATION;
ANTIGENS, CD95;
APOPTOSIS;
BCL-2-ASSOCIATED X PROTEIN;
BREAST NEOPLASMS;
CARRIER PROTEINS;
CASPASES;
CYTOCHROME C GROUP;
ENZYME ACTIVATION;
FAS LIGAND PROTEIN;
HUMANS;
MEMBRANE GLYCOPROTEINS;
MEMBRANE POTENTIALS;
MITOCHONDRIA;
NITRIC OXIDE;
PROTEIN-TYROSINE-PHOSPHATASE;
PROTO-ONCOGENE PROTEINS;
PROTO-ONCOGENE PROTEINS C-BCL-2;
REACTIVE OXYGEN SPECIES;
RNA, MESSENGER;
TUMOR CELLS, CULTURED;
UP-REGULATION;
MLCS;
MLOWN;
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EID: 0033627736
PISSN: 10196439
EISSN: None
Source Type: Journal
DOI: 10.3892/ijo.16.1.109 Document Type: Article |
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Times cited : (48)
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References (0)
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