scholarly journals Increased breast tissue receptor activator of nuclear factor-κB ligand (RANKL) gene expression is associated with higher mammographic density in premenopausal women

Oncotarget ◽  
2017 ◽  
Vol 8 (43) ◽  
pp. 73787-73792 ◽  
Author(s):  
Adetunji T. Toriola ◽  
Ha X. Dang ◽  
Ian S. Hagemann ◽  
Catherine M. Appleton ◽  
Graham A. Colditz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammographic Density ◽  
Breast Tissue ◽  
Premenopausal Women ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Receptor Activator

scholarly journals Circulating Receptor Activator of Nuclear Factor-κB (RANK), RANK ligand (RANKL), and Mammographic Density in Premenopausal Women

2018 ◽  
Vol 11 (12) ◽  
pp. 789-796 ◽  
Author(s):  
Adetunji T. Toriola ◽  
Catherine M. Appleton ◽  
Xiaoyu Zong ◽  
Jingqin Luo ◽  
Katherine Weilbaecher ◽  
...  
Keyword(s):  
Mammographic Density ◽  
Premenopausal Women ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Rank Ligand ◽  
Receptor Activator

Osteopontin is associated with nuclear factor κB gene expression during tail-suspension-induced bone loss

2006 ◽  
Vol 312 (16) ◽  
pp. 3075-3083 ◽  
Author(s):  
Muneaki Ishijima ◽  
Yoichi Ezura ◽  
Kunikazu Tsuji ◽  
Susan R. Rittling ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Loss ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Tail Suspension

scholarly journals Receptor activator of nuclear factor-κB ligand and osteoprotegerin

Cancer ◽  
2001 ◽  
Vol 92 (3) ◽  
pp. 460-470 ◽  
Author(s):  
Lorenz C. Hofbauer ◽  
Andreas Neubauer ◽  
Armin E. Heufelder
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Receptor Activator

scholarly journals Activation of Nuclear Factor κb and bcl-x Survival Gene Expression by Nerve Growth Factor Requires Tyrosine Phosphorylation of IκBα

2001 ◽  
Vol 152 (4) ◽  
pp. 753-764 ◽  
Author(s):  
Nguyen Truc Bui ◽  
Antonia Livolsi ◽  
Jean-Francois Peyron ◽  
Jochen H.M. Prehn
Keyword(s):  
Gene Expression ◽  
Tyrosine Phosphorylation ◽  
Fluorescent Protein ◽  
Nuclear Translocation ◽  
Nuclear Factor Κb ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Nuclear Factor ◽  
Human Neuroblastoma ◽  
Tnf Α

NGF has been shown to support neuron survival by activating the transcription factor nuclear factor-κB (NFκB). We investigated the effect of NGF on the expression of Bcl-xL, an anti–apoptotic Bcl-2 family protein. Treatment of rat pheochromocytoma PC12 cells, human neuroblastoma SH-SY5Y cells, or primary rat hippocampal neurons with NGF (0.1–10 ng/ml) increased the expression of bcl-xL mRNA and protein. Reporter gene analysis revealed a significant increase in NFκB activity after treatment with NGF that was associated with increased nuclear translocation of the active NFκB p65 subunit. NGF-induced NFκB activity and Bcl-xL expression were inhibited in cells overexpressing the NFκB inhibitor, IκBα. Unlike tumor necrosis factor-α (TNF-α), however, NGF-induced NFκB activation occurred without significant degradation of IκBs determined by Western blot analysis and time-lapse imaging of neurons expressing green fluorescent protein–tagged IκBα. Moreover, in contrast to TNF-α, NGF failed to phosphorylate IκBα at serine residue 32, but instead caused significant tyrosine phosphorylation. Overexpression of a Y42F mutant of IκBα potently suppressed NFG-, but not TNF-α–induced NFκB activation. Conversely, overexpression of a dominant negative mutant of TNF receptor-associated factor-6 blocked TNF-α–, but not NGF-induced NFκB activation. We conclude that NGF and TNF-α induce different signaling pathways in neurons to activate NFκB and bcl-x gene expression.

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