Biomedical Engineering Reference
In-Depth Information
[86]
De Bosscher, K., Vanden Berghe, W., Vermeulen, L. et al., Glucocorticoids repress
NF-kappaB-driven genes by disturbing the interaction of p65 with the basal tran-
scription machinery, irrespective of coactivator levels in the cell,
Proc. Natl. Acad.
Sci. USA,
97, 3919, 2000.
[87]
Nissen, R.M. and Yamamoto, K.R., The glucocorticoid receptor inhibits NFkappaB
by interfering with serine-2 phosphorylation of the RNA polymerase II carboxy-
terminal domain,
Genes Dev.,
14, 2314, 2000.
[88]
Sheppard, K.A., Phelps, K.M., Williams, A.J. et al., Nuclear integration of glucocor-
ticoid receptor and nuclear factor-kappaB signaling by CREB-binding protein and
steroid receptor coactivator-1,
J. Biol. Chem.,
273, 29291, 1998.
[89]
McKay, L.I. and Cidlowski, J.A., CBP (CREB binding protein) integrates NF-kappaB
(nuclear factor-kappaB) and glucocorticoid receptor physical interactions and antag-
onism,
Mol. Endocrinol.,
14, 1222, 2000.
[90]
Li, J., Lin, Q., Yoon, H.G. et al., Involvement of histone methylation and phospho-
rylation in regulation of transcription by thyroid hormone receptor,
Mol. Cell Biol.,
22, 5688, 2002.
[91]
Peterson, C.L. and Laniel, M.A., Histones and histone modifications,
Curr. Biol.,
14,
R546, 2004.
[92]
Ayroldi, E., Migliorati, G., Bruscoli, S. et al., Modulation of T-cell activation by the
glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor-kappaB,
Blood,
98, 743, 2001.
[93]
Franks, M.E., Macpherson, G.R., and Figg, W.D., Thalidomide,
Lancet,
363, 1802, 2004.
[94]
Sleijfer, S., Kruit, W.H., and Stoter, G., Thalidomide in solid tumours: The resurrec-
tion of an old drug,
Eur. J. Cancer,
40, 2377, 2004.
[95]
Yoshida, S., Ono, M., Shono, T. et al., Involvement of interleukin-8, vascular endo-
thelial growth factor, and basic fibroblast growth factor in tumor necrosis factor alpha-
dependent angiogenesis,
Mol. Cell. Biol.,
17, 4015, 1997.
[96]
Stephens, T.D., Bunde, C.J., and Fillmore, B.J., Mechanism of action in thalidomide
teratogenesis,
Biochem. Pharmacol.,
59, 1489, 2000.
[97]
Moreira, A.L., Sampaio, E.P., Zmuidzinas, A. et al., Thalidomide exerts its inhibitory
action on tumor necrosis factor alpha by enhancing mRNA degradation,
J. Exp. Med.,
177, 1675, 1993.
[98]
Marriott, J.B., Clarke, I.A., Dredge, K. et al., Thalidomide and its analogues have
distinct and opposing effects on TNF-alpha and TNFR2 during co-stimulation of both
CD4(+) and CD8(+) T cells,
Clin. Exp. Immunol.,
130, 75, 2002.
[99]
Keifer, J.A., Guttridge, D.C., Ashburner, B.P. et al., Inhibition of NF-kappa B activity
by thalidomide through suppression of IkappaB kinase activity,
J. Biol. Chem.,
276,
22382, 2001.
[100]
Epinat, J.C. and Gilmore, T.D., Diverse agents act at multiple levels to inhibit the
Rel/NF-kappaB signal transduction pathway,
Oncogene,
18, 6896, 1999.
[101]
Bowie, A. and O'Neill, L.A., Oxidative stress and nuclear factor-kappaB activation:
A reassessment of the evidence in the light of recent discoveries,
Biochem. Pharma-
col.,
59, 13, 2000.
[102]
Rahman, I., Marwick, J., and Kirkham, P., Redox modulation of chromatin remod-
eling: Impact on histone acetylation and deacetylation, NF-kappaB and pro-inflam-
matory gene expression,
Biochem. Pharmacol.,
68, 1255, 2004.
[103]
Hensley, K., Robinson, K.A., Gabbita, S.P. et al., Reactive oxygen species, cell
signaling, and cell injury,
Free Radic. Biol. Med.,
28, 1456, 2000.
