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Nuclear factor kappaB function

Kim, G.Y., Kim, J.H., Ahn, S.C. et al. 2004. Lycopene suppresses the lipopolysaccharide-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and nuclear factor-kappaB. Immunology 113 203-211. [Pg.480]

Thomas RK, Sos ML, Zander T, Mani O, Popov A, Berenbrinker D, Smola-Hess S, Schultze JL, Wolf J. 2005. Inhibition of nuclear translocation of nuclear factor-kappaB despite lack of functional IkappaBalpha protein overcomes multiple defects in apoptosis signaling in human B-cell malignancies. Clin Cancer Res 11 8186-8194. [Pg.397]

Ravati A, Ahlemeyer B, Becker A, Klumpp S, Krieglstein J (2001) Preconditioning-induced neuroprotection is mediated by reactive oxygen species and activation of the transcription factor nuclear factor-kappaB. J Neurochem 78 909-919 Ray A, Prefontaine KE (1994) Physical association and functional antagonism between the p65 subunit of transcription factor NF-kappa B and the glucocorticoid receptor. Proc Natl Acad Sci USA 91 752-756... [Pg.315]

Lewis J, et al. Disruption of hsp90 function results in degradation of the death domain kinase, receptor-interacting protein (RIP), and blockage of tumor necrosis factor-induced nuclear factor-kappaB activation. J. Biol. Chem. 2000 275 10519-10526. Lee TH, et al. The kinase activity of Ripl is not required for tumor necrosis factor-alpha-induced IkappaB kinase or p38 MAP kinase activation or for the ubiquitination of Ripl by Traf2. J. Biol. Chem. 2004 279 33185-33191. [Pg.183]

Since an extreme pro-oxidant status of a cell can lead to a progressive loss of cellular function and eventual death, cells have developed mechanisms to detect changes in the redox status of cells. These switches are used to regulate and turn on the antioxidant machinery of the cell. These signals are largely mediated by redox-sensitive transcription factors. Although a large number of very extensively studied transcription factors are now know to respond to redox status, nuclear factor-kappaB (NF-kB) deserves special mention. NF-kB usually resides in the... [Pg.1907]

Hang CH, Chen G, Shi JX, Zhang X, Li JS (2006) Cortical expression of nuclear factor kappaB after human brain contusion. Brain Res 1109 14-21 Harris LK, Black RT, Golden KM, Reeves TM, PovUshack JT, Phillips LL (2001) Traumatic brain injury-induced changes in gene expression and functional activity of mitochondrial cytochrome C oxidase. J Neurotrauma 18 993-1009... [Pg.213]

Stehlik C, de Martin R, Kumabashiri I, Schmid JA, Binder BR, Lipp J (1998) Nuclear factor (NF)-kappaB-regulated X-chromosome-linked iap gene expression protects endothelial cells from tumor necrosis factor alpha-induced apoptosis. J Exp Med 188 211-216 Stennicke HR, Deveraux QL, Humke EW, Reed JC, Dixit VM, Salvesen GS (1999) Caspase-9 ctin be activated without proteolytic processing. J Biol Chem 274 8359-8362 Sun XM, Butterworth M, MacFarlane M, Dubiel W, Ciechanover A, Cohen GM (2004) Caspase activation inhibits proteasome function during apoptosis. Mol Cell 14 81-93 Suzuki Y, Imai Y, Nakayama H, Takahashi K, Takio K, Takahashi R (2001) A serine protease, HtrA2, is released from the mitochondria and interacts with XIAP, inducing cell death. Mol Cell 8 613-621... [Pg.45]

Khorooshi R, Babcock AA, Owens T (2008) NF-kappaB-driven STAT2 and CCL2 expression in astrocytes in response to brain injury. J Immunol 181 7284-7291 Kim GM, Xu J, Xu JM, Song SK, Yan P Ku G, Xu XM, Hsu CY (2001) Tumor necrosis factor receptor deletion reduces nuclear factor-kappa B activation, cellular inhibitor of apoptosis protein 2 expression, and functional recovery after traumatic spinal cord injury. J Neurosci 21 6617-6625... [Pg.213]


See other pages where Nuclear factor kappaB function is mentioned: [Pg.333]    [Pg.255]    [Pg.2808]    [Pg.87]    [Pg.82]    [Pg.274]    [Pg.55]    [Pg.232]    [Pg.1867]    [Pg.143]    [Pg.360]   
See also in sourсe #XX -- [ Pg.83 ]




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