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IKBKB — IL1A

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: IKBKB → IL1A (increases, IL1A Activity) Prajapati et al., J Biol Chem 2004*
  Evidence: The NF-kappaB pathway is important in the control of the immune and inflammatory response. One of the critical events in the activation of this pathway is the stimulation of the IkappaB kinases (IKKs) by cytokines such as tumor necrosis factor-alpha and interleukin-1.
• OpenBEL Selventa BEL large corpus: IKBKB → IL1A (increases, IL1A Activity) Peters et al., Mol Cell 2000*
  Evidence: This led to the identification of a high molecular weight IkBalpha kinase complex capable of phosphorylating IkBalpha specifically on serines 32 and 36. Subsequently, the same complex was isolated from TNFalpha-induced HeLa cells and found to contain two IkBalpha kinases, designated IKKalpha and IKKbeta (or IKK1 and IKK2). These kinases were cloned and shown to be activated by TNFalpha, IL-1, and PMA.

Text-mined interactions from Literome

Aupperle et al., J Immunol 1999 (Arthritis, Rheumatoid) : IKK activity in both RA and osteoarthritis FLS was strongly induced by TNF-alpha and IL-1 in a concentration dependent manner
Kamthong et al., Biochem J 2001 : The results show that the level of IKK protein remains constant in the presence of cAMP, forskolin and/or IL-1, whereas IKK activity was robustly stimulated by IL-1 ... Nonetheless, dibutyryl-cAMP or forskolin did not affect the IKK activation induced by IL-1
Chen et al., J Biol Chem 2002 : Under these conditions or upon overexpression of wild type Akt, IL-1beta induced IKKbeta activity is diminished
Makris et al., Mol Cell Biol 2002 : Substitution of two leucines within a C-terminal leucine zipper motif markedly reduced IKK activation by TNF-alpha and IL-1 ... Another point mutation resulting in a cysteine-to-serine substitution within the putative Zn finger motif affected IKK activation by TNF-alpha but not by IL-1
Broemer et al., Oncogene 2004 (Inflammation...) : Short-time inhibition of Hsp90 resulted in impaired IKK kinase activation by TNFalpha, IL-1beta or phorbolester PMA
Li et al., Acta Pharmacol Sin 2006 (Pulmonary Disease, Chronic Obstructive) : NAC inhibited the phosphorylation of IKKbeta, IKK alpha, and IkappaB alpha induced by TNF-a, but had no effect on the phosphorylation of IKKbeta , IKK alpha and IkappaB alpha induced by IL-1
Besse et al., J Biol Chem 2007 : A green fluorescent protein fusion protein containing the last 100 residues of TAK1 ( TAK1-C100 ) abolished the interaction of endogenous TAB2/TAB3 with TAK1, the phosphorylation of TAK1, and prevented the activation of IKK and MAPK induced by IL-1 , TNF, and RANKL
Besse et al., Biochem Biophys Res Commun 2007 : Stable expression of TRIP or a RING mutant did not affect IKK activation induced by TNF or IL-1 and had no affect on TNF induced apoptosis
Chang et al., Nat Immunol 2009 (Inflammation) : Peli1 was required for TLR3 induced activation of IkappaB kinase (IKK) and its ` downstream ' target, transcription factor NF-kappaB, but was dispensable for IKK-NF-kappaB activation induced by several other TLRs and the interleukin 1 (IL-1) receptor
Fan et al., Cell Signal 2011 : TAK1 Lys-158 but not Lys-209 is required for IL-1ß induced Lys63 linked TAK1 polyubiquitination and IKK/NF-?B activation ... Lys63 linked polyubiquitination of TAK1 is required for IL-1ß induced IKK/NF-?B activation ... Here we report that TAK1 Lysine 158 but not Lysine 209 is required for IL-1ß induced Lys63 linked TAK1 polyubiquitination and TAK1 mediated IKK , JNK, and p38 activation ... Reconstitution of TAK1-deficient mouse embryo fibroblast cells with wild-type, K158R mutant, or K209R mutant TAK1 reveals that TAK1 Lys-158 but not Lys-209 is required for IL-1ß induced IKK , p38 and JNK activation
Buhrmann et al., J Biol Chem 2011 (Inflammation) : Curcumin suppressed IL-1ß induced PI-3K p85/Akt activation and its association with IKK
Ling et al., Cancer Cell 2012 (Carcinoma, Pancreatic Ductal...) : KrasG12D induced IKK2/ß/NF-?B activation by IL-1a and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma
Rafferty et al., Cell Immunol 2012 : ROCK inhibition also suppressed IL-1 induced JNK phosphorylation in both cell lines, but high levels of the inhibitor had no significant effect on IL-1 stimulated Caco-2 I?Ba phosphorylation and degradation or IKK phosphorylation and kinase activity
Geleziunas et al., Mol Cell Biol 1998 (Cell Transformation, Viral...) : Our studies now demonstrate that HTLV-1 Tax activates the recently identified cellular kinases IkappaB kinase alpha (IKKalpha) and IKKbeta , which normally phosphorylate IkappaB alpha on both of its N-terminal regulatory serines in response to tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) stimulation