Deletion of Glu155 causes a deficiency of glutathione transferase Omega 1-1 but does not alter sensitivity to arsenic trioxide and other cytotoxic drugs

• Published in: The international journal of biochemistry & cell biology Vol. 40; no. 11; pp. 2553 - 2559
• Main Authors: Schmuck, Erica, Cappello, Jean, Coggan, Marjorie, Brew, Jenny, Cavanaugh, Juleen A., Blackburn, Anneke C., Baker, Rohan T., Eyre, Helen J., Sutherland, Grant R., Board, Philip G.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 2008
• Subjects: Antineoplastic Agents - metabolism; Arsenic biotransformation; Arsenicals - metabolism; Cell Line, Tumor; Cytotoxins - metabolism; Drug resistance; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Genotype; Glutamic Acid - metabolism; Glutathione Transferase - deficiency; Glutathione Transferase - genetics; Glutathione transferase Omega; Glutatione transferase deficiency; GSTO1-1; Humans; Oxides - metabolism; Polymorphism, Genetic; Glutathione transferase Omega; FBS; FISH; DAPI; Arsenic biotransformation; Drug resistance; Glutatione transferase deficiency; GSTO1-1

The Omega class glutathione transferase GSTO1-1 can catalyze the reduction of pentavalent methylated arsenic species and is responsible for the biotransfomation of potentially toxic α-haloketones. We investigated the cause of GSTO1-1 deficiency in the T-47D breast cancer cell line and found that the...