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NFKB1 — POLDIP2

Text-mined interactions from Literome

Garrett et al., Biochim Biophys Acta 1999 (Precursor B-Cell Lymphoblastic Leukemia-Lymphoma) : In CD14 transfected 70Z/3 pre-B lymphocyte tumor cells, these responses include activation of the MAP kinase homolog, p38 , activation of NF-kappaB , and transcription of kappa light chains, leading to the assembly of surface IgM
Haas et al., J Biol Chem 1999 : These cells show a permanent activation of the transcription factor NF-kappaB , exert constitutive p38 mitogen activated protein kinase activity, and produce high amounts of interleukin-6
Taher et al., Biochemistry 2000 : Inhibition of NF-kappa B activation by the protease inhibitor N-alpha-tosyl-L-phenylalanine chloromethyl ketone ( TPCK ) prevents UV activation of HIV gene expression, but does not inhibit p38 MAP kinase activation
Morigiwa et al., Nihon Yakurigaku Zasshi 2000 : Release of cytokines may be induced via Ca2+ influx and activation of NFAT, NF-kappa B or p44/42 and p38 MAP kinases, switching off the mitotic signal transduction pathway and triggering the apoptotic cascade at the same time
Zaheer et al., Neurochem Res 2001 : The activations of CREB and NF-kappaB were blocked by inhibitors of either p38 ( SB-203580 ) or MEK ( PD-098059 ), suggesting that they were events downstream of MAK kinase
Hagood et al., Am J Respir Cell Mol Biol 2002 : IL-1beta induces DNA binding of both nuclear factor kappaB (NF-kappaB) and CAATT-enhancer binding protein (C/EBP), and activation of p38 mitogen activated protein kinase in both subpopulations
Roberts et al., Cryobiology 2002 : Inhibition of MAPK with an MEK inhibitor ( PD098059 ) blocked the activation of NF-kappaB but a specific p38 inhibitor ( SB203580 ) had no effect on NF-kappaB
Park et al., Science 2002 (MAP Kinase Signaling System...) : Because macrophages that are deficient in transcription factor nuclear factor kappaB (NF-kappaB) are also sensitive to activation induced death and p38 is required for expression of certain NF-kappaB target genes, p38 is probably essential for synergistic induction of those NF-kappaB target genes that prevent apoptosis of activated macrophages
Ajmone-Cat et al., J Neurochem 2003 : In LPS activated microglia, PS-liposomes did not affect NF-kappaB activation but inhibited the phosphorylation of p38 and delayed that of CREB
Wong et al., Am J Respir Cell Mol Biol 2003 : The phosphorylation of inhibitor kappaB-alpha and p38 mitogen activated protein kinase ( MAPK ) was detected by Western blot, whereas NF-kappaB activity was measured by electrophoretic mobility shift assay
Jefferies et al., Immunol Lett 2004 : Further investigation into the role of Btk in LPS signalling has directly implicated Btk downstream of TLR4, both with respect to p38 MAPK activation and activation of the transcription factor NFkappaB
Tian et al., Blood 2005 (Lymphoma, B-Cell) : Induction of Bcl10 activity caused rapid activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK), but not activation of extracellular signal regulated kinase ( ERK ) or p38 mitogen activated protein ( MAP ) kinases
Davies et al., Mol Cell Biol 2005 : In fibroblasts lacking TRAF2 or in carcinoma cells in which TRAF2 has been depleted by RNA interference, the CD40 mediated activation of NF-kappaB and JNK is significantly reduced, and the activation of p38 and Akt is severely impaired
Madonna et al., Int J Immunopathol Pharmacol 2007 : Co-treatment of HUVEC with insulin and SB202190 strongly reverted the stimulatory effect of insulin on NF-KB activation, thus establishing a link between NF-KB activation and p38MAPkinase mediated induction of VCAM-1 by insulin
Zhou et al., World J Gastroenterol 2008 (Adenocarcinoma...) : Viable LBG or LBG- ( s ) pretreatment attenuated the expression of TLR4, inhibited the phosphorylation of TAK1 and p38MAPK , prevented the activation of NF-kappaB , and consequently blocked IL-8 production
Hastings et al., Arterioscler Thromb Vasc Biol 2009 (Atherosclerosis) : Neutralization of the IL-8 receptor, CXCR2, further induced VCAM-1 in the presence of IL-1beta, and phospho-p38 was required for NF-kappaB activation and VCAM-1 expression
Ci et al., Fundam Clin Pharmacol 2009 (Inflammation) : Signal transduction studies showed that avermectin significantly inhibits NF-kappaB p65 translocation into the nucleus and inhibits JNK and p38 phosphorylation protein expression
Qi et al., Br J Pharmacol 2009 : Further, inhibition of p38 mitogen activated protein kinases ( MAPKs ) significantly suppressed IFN-gamma induced MDC expression and NF-kappaB activation
Zechner et al., J Biol Chem 1998 : Additionally, while NF-kappaB is activated in myocardial cells by p38 , this does not appear to be the major mechanism by which MKK6 ( Glu ) exerts its anti-apoptotic effects in this cell type, suggesting a novel pathway for p38 mediated protection from apoptosis