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Constitutive BR3 receptor signaling in diffuse, large B-cell
lymphomas stabilizes nuclear factor-κB–inducing kinase
while activating both canonical and alternative nuclear
factor-κB pathways
by Lan V. Pham, Lingchen Fu, Archito T. Tamayo, Carlos Bueso-Ramos, Elias
Drakos, Francisco Vega, L. Jeffrey Medeiros, and Richard J. Ford
Blood
Volume 117(1):200-210
January 6, 2011
©2011 by American Society of Hematology
Identification and characterization of NF-κB family members in DLBCL subsets.
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
Immunohistochemical analysis of NF-κB components in DLBCL cell lines and primary DLBCL
samples.
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
NF-kB DNA-binding analysis in DLBCL cell lines and primary samples.
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
NIK kinase protein accumulates in DLBCL tumor cells.
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
BR3 receptor activation promotes DLBCL cell growth through NIK protein stabilization.
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
The role of TRAF3 in the stabilization of NIK in DLBCL cells.
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
Constitutive BLyS/BR3 signaling activates NIK-induced NF-κB pathway activation through
induction of TRAF3 degradation in DLBCL. (A) Cytoplasmic cell lysates from MS-GCB or HBABC DLBCL cells were immunoprecipitated with BR3 or TRAF3 antibodies and probed wi...
Lan V. Pham et al. Blood 2011;117:200-210
©2011 by American Society of Hematology
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