Intracellular oxidation/reduction status in the regulation of transcription factors NF-κB and AP-1

Gius, David; Botero, Anna; Shah, Sunita; Curry, Heather A.

doi:10.1016/s0378-4274(99)00024-7

Cited by 245 publications

(194 citation statements)

References 90 publications

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“…lating results in literature (47,48) and our previous reports (5,22) have demonstrated that ionizing radiation enhances NF-B DNA binding and transcriptional activities that are associated with reduced cell radiosensitivity. To get insight of the network of NF-B-mediated radioprotection, the activity of a group of MAPKs was measured in irradiated breast carcinoma MCF-7 cells.…”

Section: Ir Activates Nf-b and Erk But Not P38 Or Jnk-accumu-supporting

confidence: 54%

Co-activation of ERK, NF-κB, and GADD45β in Response to Ionizing Radiation

Wang

Dong

et al. 2005

Journal of Biological Chemistry

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Section: Ir Activates Nf-b and Erk But Not P38 Or Jnk-accumu-supporting

confidence: 54%

Co-activation of ERK, NF-κB, and GADD45β in Response to Ionizing Radiation

Wang

Dong

et al. 2005

Journal of Biological Chemistry

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“…C-Jun expression has been shown to promote entry into S-phase in the absence of mitogenic stimulation [48,61] and substantial evidence shows that it is redox regulated (reviewed by [62]. Figure 4 shows that cells that overexpress xCT have increased signaling through AP-1 even in the presence of calcium channel antagonists.…”

Section: Discussionmentioning

confidence: 99%

xCT expression reduces the early cell cycle requirement for calcium signaling

Lastro

Kourtidis

Farley

et al. 2008

Cellular Signalling

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Calcium has long been recognized as an important regulator of cell cycle transitions although the mechanisms are largely unknown. A functional genomic screen has identified genes involved in the regulation of early cell cycle progression by calcium. These genes when overexpressed confer the ability to bypass the G1/S arrest induced by Ca 2+ -channel antagonists in mouse fibroblasts. Overexpression of the cystine-glutamate exchanger, xCT, had the greatest ability to evade calcium antagonist-induced cell cycle arrest. xCT carries out the rate limiting step of glutathione synthesis in many cell types and is responsible for the uptake of cystine in most human cancer cell lines. Functional analysis indicates that the cystine uptake activity of xCT overcomes the G1/S arrest induced by Ca 2+ -channel antagonists by bypassing the requirement for calcium signaling. Since cells overexpressing xCT were found to have increased levels and activity of the AP-1 transcription factor in G1, redox stimulation of AP-1 activity accounts for the observed growth of these cells in the presence of calcium channel antagonists. These results suggest that reduced calcium signaling impairs AP-1 activation and that xCT expression may directly affect cell proliferation.

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“…This dimeric transcription factor is composed of different members of the Rel family -p65 (RelA), p50, p52, c-Rel and RelB (Baeuerle and Baltimore, 1996;Barkett and Gilmore, 1999) -which can activate a great variety of genes involved in stress responses, inflammation and programmed cell death (apoptosis) (Baeuerle and Baltimore, 1996). Numerous experiments indicate that NF-kB is actively involved in the signaling network of apoptotic/ antiapoptotic responses induced by ionizing radiation (IR) and oxidative stress (Baldwin, 1996;Barkett and Gilmore, 1999;Gius et al, 1999;Granville et al, 2000;Bradbury et al, 2001;Kurland and Meyn, 2001;Ravi et al, 2001;McBride et al, 2002). With binding sites found in the gene control region of about 150 stress-responsive effector genes, the major function of NF-kB activation is believed to reduce the apoptotic process via activation of antiapoptosis genes (Barkett and Gilmore, 1999).…”

Section: Introductionmentioning

confidence: 99%

Expression of ErbB2 enhances radiation-induced NF-κB activation

et al. 2004

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Her-2/neu (ErbB2) oncogene, the second member of the epidermal growth factor receptor (EGFR) family, encodes a transmembrane tyrosine kinase receptor in Her-2-positive tumors. Accumulating evidences demonstrate that signaling networks activated by EGFR and transcription factor NFjB are associated with cell response to ionizing radiation (IR). The present study shows that overexpression of ErbB2 enhanced NF-jB activation induced by IR in human breast carcinoma MCF-7 cells transfected with ErbB2 genes (MCF-7/ErbB2). Stable transfection of dominantnegative mutant IjB (MCF-7/ErbB2/mIjB) or treatment with anti-ErbB2 antibody, Herceptin, inhibited NF-jB activation and radiosensitized MCF-7/ErbB2 cells. Consistent with NF-jB regulation, basal and IR-induced Akt, a kinase downstream of ErbB2, was activated in MCF-7/ ErbB2 cells and inhibited by Herceptin. To identify specific genes affected by ErbB2-mediated NF-jB activation, a group of IR-responsive elements Cyclin B1, Cyclin D1, Bcl-2, Bcl/XL, BAD and BAX were evaluated. Basal levels of prosurvival elements Cyclin B1, Cyclin D1, Bcl-2 and Bcl/XL but not apoptotic BAD and BAX were upregulated in MCF-7/ErbB2 cells with striking enhancements in Bcl-2 and Bcl/XL. IR further induced Cyclin B1 and Cyclin D1 expression that was reduced by Herceptin. Bcl-2 kept a high steady level after Herceptin þ IR treatment and, in contrast to control MCF-7/Vector cells, Bcl/XL was inhibited in MCF-7/ErbB2 cells by Herceptin þ IR treatment. However, all four prosurvival proteins were downregulated by inhibition of NF-jB in MCF-7/ErbB2/mIjB cells. These results thus provide evidence suggesting that overexpression of ErbB2 is able to enhance NF-jB response to IR, and that a specific prosurvival network downstream of NF-jB is triggered by treatments using anti-ErbB2 antibody combined with radiation.

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Intracellular oxidation/reduction status in the regulation of transcription factors NF-κB and AP-1

Cited by 245 publications

References 90 publications

Co-activation of ERK, NF-κB, and GADD45β in Response to Ionizing Radiation

Co-activation of ERK, NF-κB, and GADD45β in Response to Ionizing Radiation

xCT expression reduces the early cell cycle requirement for calcium signaling

Expression of ErbB2 enhances radiation-induced NF-κB activation

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