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- W2228076217 abstract "An excess in the levels of reactive oxygen species (ROS) can contribute to the development of cancer due to the oxidative damage to molecules such as DNA, protein and cellular membranes. Antioxidant proteins, including those that belong to the glutathione peroxidase (GPx), superoxide dismutase (SOD) and thioredoxin reductase (TrxR) families, contribute to the maintenance of the cellular redox balance by detoxification of ROS. Our attention was drawn to a report indicating that the non-receptor tyrosine kinase c-Abl could phosphorylate and activate the activity of GPx1 in tissue culture cells. To investigate this phenomenon further in humans, GPx activity were determined in samples obtained from patients with chronic myelogenous leukemia (CML), a disease initiated by the rearrangement of two different chromosomes and resulting in the Bcr-Abl oncogene. Samples were obtained before and after treatment with the Bcr-Abl inhibitor imatinib mesylate, and of the seven patient sample sets obtained, four exhibited elevated GPx activity following treatment, which was contrary to expectation. In order to expand upon this observation, the CML established cell lines KU812 and MEG-01 were treated with imatinib and the effect on several antioxidant proteins was determined. The levels of GPx1, manganese superoxide dismutase (MnSOD) and thioredoxin reductase 1 (TrxR1) were each significantly increased following treatment with imatinib. This increase was not due to altered steady-state mRNA levels, and appeared to be dependent on the expression of Bcr-Abl, as no increases were observed following imatinib treatment of cells that did not express the fusion protein. The nutrient-sensing signaling protein, mammalian target of rapamycin (mTOR), can be activated by Bcr-Abl and its activity regulates the translation of several proteins. Treatment of those same cells used in the imatinib studies with rapamycin, an inhibitor of mTOR, resulted in elevated GPx1, TrxR1 and GPx4 protein levels independent of Bcr-Abl expression. These proteins all belong to the selenoprotein family of peptides that contain the UGA-encoded amino acid selenocysteine. Collectively, these data provide evidence of a novel means of regulating antioxidants of the selenoprotein family via the mTOR pathway." @default.
- W2228076217 created "2016-06-24" @default.
- W2228076217 creator A5016734697 @default.
- W2228076217 date "2013-06-28" @default.
- W2228076217 modified "2023-09-23" @default.
- W2228076217 title "The Post-Transcriptional Regulation of Antioxidant Enzymes" @default.
- W2228076217 cites W1480352152 @default.
- W2228076217 cites W1484180915 @default.
- W2228076217 cites W1489777708 @default.
- W2228076217 cites W1490860457 @default.
- W2228076217 cites W1491060698 @default.
- W2228076217 cites W1517703574 @default.
- W2228076217 cites W1540141309 @default.
- W2228076217 cites W1543996619 @default.
- W2228076217 cites W1544230661 @default.
- W2228076217 cites W1548811121 @default.
- W2228076217 cites W1556218239 @default.
- W2228076217 cites W1565745037 @default.
- W2228076217 cites W1573826674 @default.
- W2228076217 cites W1577832196 @default.
- W2228076217 cites W1640740682 @default.
- W2228076217 cites W1781125152 @default.
- W2228076217 cites W1864601388 @default.
- W2228076217 cites W188687039 @default.
- W2228076217 cites W1907184865 @default.
- W2228076217 cites W1920447185 @default.
- W2228076217 cites W1939249492 @default.
- W2228076217 cites W1940436875 @default.
- W2228076217 cites W1955468565 @default.
- W2228076217 cites W1963668163 @default.
- W2228076217 cites W1965941075 @default.
- W2228076217 cites W1966597352 @default.
- W2228076217 cites W1966815619 @default.
- W2228076217 cites W1966920840 @default.
- W2228076217 cites W1967099953 @default.
- W2228076217 cites W1967926175 @default.
- W2228076217 cites W1968276731 @default.
- W2228076217 cites W1968996242 @default.
- W2228076217 cites W1969436148 @default.
- W2228076217 cites W1970094644 @default.
- W2228076217 cites W1970416169 @default.
- W2228076217 cites W1970841988 @default.
- W2228076217 cites W1970965314 @default.
- W2228076217 cites W1970967418 @default.
- W2228076217 cites W1971402937 @default.
- W2228076217 cites W1971510265 @default.
- W2228076217 cites W1973744965 @default.
- W2228076217 cites W1973821902 @default.
- W2228076217 cites W1974047460 @default.
- W2228076217 cites W1974126557 @default.
- W2228076217 cites W1976194065 @default.
- W2228076217 cites W1976842211 @default.
- W2228076217 cites W1977540067 @default.
- W2228076217 cites W1977990240 @default.
- W2228076217 cites W1978240770 @default.
- W2228076217 cites W1978668880 @default.
- W2228076217 cites W1978955254 @default.
- W2228076217 cites W1979175943 @default.
- W2228076217 cites W1979200514 @default.
- W2228076217 cites W1979456040 @default.
- W2228076217 cites W1980023909 @default.
- W2228076217 cites W1980520537 @default.
- W2228076217 cites W1983311902 @default.
- W2228076217 cites W1983397667 @default.
- W2228076217 cites W1983698019 @default.
- W2228076217 cites W1984568177 @default.
- W2228076217 cites W1985501344 @default.
- W2228076217 cites W1985797100 @default.
- W2228076217 cites W1986139301 @default.
- W2228076217 cites W1987338970 @default.
- W2228076217 cites W1992249063 @default.
- W2228076217 cites W1992527366 @default.
- W2228076217 cites W1993763219 @default.
- W2228076217 cites W1994977897 @default.
- W2228076217 cites W1995412458 @default.
- W2228076217 cites W1996439981 @default.
- W2228076217 cites W1996604197 @default.
- W2228076217 cites W1997208169 @default.
- W2228076217 cites W1998146257 @default.
- W2228076217 cites W1998994062 @default.
- W2228076217 cites W2000017694 @default.
- W2228076217 cites W2002209113 @default.
- W2228076217 cites W2002245246 @default.
- W2228076217 cites W2002304768 @default.
- W2228076217 cites W2002990742 @default.
- W2228076217 cites W2003018523 @default.
- W2228076217 cites W2005105190 @default.
- W2228076217 cites W2006110932 @default.
- W2228076217 cites W2006313098 @default.
- W2228076217 cites W2006633852 @default.
- W2228076217 cites W2007134361 @default.
- W2228076217 cites W2007202879 @default.
- W2228076217 cites W2007565925 @default.
- W2228076217 cites W2007825194 @default.
- W2228076217 cites W2008532612 @default.
- W2228076217 cites W2008581655 @default.
- W2228076217 cites W2008888284 @default.
- W2228076217 cites W2009588836 @default.
- W2228076217 cites W2011346454 @default.
- W2228076217 cites W2011846287 @default.