◀ Back to NFKB1

BTK — NFKB1

Text-mined interactions from Literome

Bajpai et al., J Exp Med 2000 (Immunologic Deficiency Syndromes) : Thus, BTK is essential for activation of NF-kappaB via the B cell receptor
Khan et al., Immunol Res 2001 (Agammaglobulinemia) : Furthermore, BTK dependent activation of NF-kappaB is essential for reprogramming the expression of genes that control B cell survival and proliferation
Kaku et al., Int Immunol 2002 : We infer from these results that activation of Btk , PI-3 kinase and PKC play, at least in part, important roles in the induction of NF-kappaB in CD38 stimulated murine B cells
Jefferies et al., J Biol Chem 2003 : In addition, a dominant negative form of Btk inhibited TLR4 mediated activation of a nuclear factor kappaB (NFkappaB) dependent reporter gene in HEK293 cells as well as LPS induced activation of NFkappaB in the astrocytoma cell line U373 and the monocytic cell line RAW264.7 ... Further investigation revealed that the Btk-specific inhibitor, LFM-A13, inhibited the activation of NFkappaB by LPS in THP-1 cells
Schmidt et al., J Immunol 2006 : This phenotype correlates with Btk dependent induction of NF-kappaB and AP-1 DNA binding activity, and altered commensal bacteria populations
Doyle et al., J Biol Chem 2007 (Agammaglobulinemia...) : We demonstrate that Btk is required for NFkappaB activation, participating in the pathway to increased phosphorylation of p65 on serine 536 activated by TLR8 and TLR9
Lee et al., J Biol Chem 2008 : The lack of Btk signaling affects the activation of NFkappaB and impairs the translocation of the p65RelA subunit to the nucleus of B cells upon TLR9 stimulation ... Thus, Btk plays an important role in TLR9 signaling and acts separately to regulate NFkappaB RelA activation as well as IL-10 and IL-12 production in B cells
Matsuda et al., Blood 2009 : Nevertheless, both PI3K and Btk are required for the activation of NF-kappaB , a critical transcription factor family for B-cell development and function
Vose et al., Am J Hematol 2012 (Asymptomatic Diseases...) : At the time of relapse, agents directed at activated pathways in MCL cells such as bortezomib ( NFkB inhibitor ), BTK inhibitors or CAL-101 ( B-cell receptor inhibitors ) or lenalidamide ( antiangiogenesis ) have clinical activity in MCL patients