Gene interactions and pathways from curated databases and text-mining

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RELA — RELB

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Xia et al., Mol Cell Biol 1999 (Inflammation) : RelB , a member of this family, has been characterized as a transcription activator and is involved in the constitutive NF-kappaB activity in lymphoid tissues
Bren et al., Oncogene 2001 : Transcription of the RelB gene is regulated by NF-kappaB ... RelA is alone sufficient to induce RelB gene transcription and to mediate the stimuli-driven increase in RelB transcription
Haddad et al., J Pharmacol Exp Ther 2002 (Inflammation...) : Whereas selective inhibition of PDEs 1, 3, and 4, by the action of 8-methoxymethyl-3-isobutyl-1-methylxanthine, amrinone, and rolipram, respectively, exhibited a tendency to augment the translocation of NF-kappaB ( 1 ) ( p50 ), RelA ( p65 ), RelB ( p68 ), and c-Rel ( p75 ), selective blockade of PDE 5, 6, and 9, by the action of 4- [ [ 3',4'- ( methylenedioxy ) benzyl ] amino ] -6-methoxyquinazoline and zaprinast, attenuated lipopolysaccharide-endotoxin (LPS) mediated NF-kappaB translocation
Valéro et al., J Immunol 2002 (Autoimmune Diseases...) : Upon TNF induced activation of NZB thymocytes, nuclear translocation and DNA binding of RelA- and RelB dependent NF-kappaB heterodimers are significantly reduced
Marienfeld et al., J Biol Chem 2003 : Furthermore, electrophoretic mobility shift analysis revealed that in vitro translated RelB impaired the DNA binding activity of RelA and that overexpressed RelB significantly reduced tumor necrosis factor-alpha induced RelA activity in murine embryonic fibroblasts
Derudder et al., J Biol Chem 2003 : LTbetaR induced binding of RelB/p50 requires processing of p100 that is mediated by IKKalpha but is independent of IKKbeta, NEMO/IKKgamma, and RelA
Sivakumar et al., J Exp Med 2003 : Moreover, NF-kappa B-inducing kinase (NIK) was required for both constitutive thymic DNA binding of RelB and the specific induction of RelB complexes in vitro
Monaco et al., Proc Natl Acad Sci U S A 2004 (Arteriosclerosis...) : We found that NF-kappa B is activated in these cells and that this activity involves p65, p50, and c-Rel but not p52 or RelB
Yan et al., Immunol Cell Biol 2005 : VLP induced induction of costimulatory molecule expression, RelB activation and cytokine secretion by DC was blocked by inhibition of NF-kappaB activation, heparin or TLR4 mAb
Ruben et al., Genes Dev 1992 : Transfection experiments demonstrate that I-Rel suppresses NF-kappa B-induced transcription, probably through its association with p50
Iwamoto et al., Tohoku J Exp Med 2005 (Body Weight...) : Supershift assays with specific antibodies revealed that p50, but not p52, p65, Rel B , or c-Rel, may be involved in the activation of NF-kappaB , though the component primarily responsible for the increase could not be determined
Jacque et al., Proc Natl Acad Sci U S A 2005 : Remarkably, we show that RelA serine-276, the phosphorylation of which is induced by TNF receptor ligation, is crucial for RelA/RelB complex formation and subsequent inhibition of RelB DNA binding
Starkey et al., Diabetes 2006 (Diabetes Mellitus, Experimental) : Cytosolic content of NF-kappaB canonical pathway proteins did not differ between experimental groups after 3 months of diabetes, while NF-kappaB noncanonical pathway proteins were affected, including increased phosphorylation of inhibitor of kappaB kinase-alpha and several fold increases in NF-kappaB inducing kinase and RelB , which were predominantly located in tubular epithelial cells
Eisner et al., FEBS Lett 2006 : Supershift analysis revealed that p65 and RelB ( but not p50, p52 or cRel ) were involved in the binding of NFkappaB to DNA
Martucci et al., J Leukoc Biol 2007 : The transcription factor NF-kappaB is a central regulator of immunity, and of the NF-kappaB family, RelB is particularly involved in the expression of genes important in immune responses
Schumann et al., Proc Natl Acad Sci U S A 2007 : Up-regulation of FLIP enhanced NF-kappaB activity via NF-kappaB inducing kinase and RelB
Wang et al., Nat Cell Biol 2007 (Breast Neoplasms...) : ERalpha signalling reduced levels of functional NF-kappaB and Fra-2 AP-1 and inhibited de novo RelB synthesis, leading to an inverse correlation between RELB and ERalpha gene expression in human breast cancer tissues and cell lines
Sanz et al., PloS one 2010 : TWEAK, but not TNFalpha used as control ), induced a delayed increase in CCL21a mRNA ( 3.5+/-1.22-fold over control ) and CCL21 protein ( 2.5+/-0.8-fold over control ), which was prevented by inhibition of the proteasome, or siRNA targeting of NIK or RelB , but not by RelA inhibition with parthenolide
Liu et al., Bing Du Xue Bao 2013 : Further investigations indicated that RelB not only promoted the Vpr mediated activation of NF-kappaB reporter gene, but also enhanced the transactivation of HIV LTR
Altaf et al., Inflammopharmacology 2013 : Inhibition by sc-514 of RelA , c-rel and p50 expression occurred with all four particles, p52 was decreased for all diamond particles ( but not CoCr ) and RelB was not inhibited with any of the particles
Weih et al., Oncogene 1994 : Although RelB protein is present at significantly lower levels in thymus and spleen extracts when compared to RelA, in both tissues the predominant kappa B-binding activity consists of p50/RelB and p52/RelB heterodimers and only very little binding of RelA containing complexes to kappa B sites was detected
Weih et al., J Exp Med 1997 (Abnormalities, Multiple...) : These results indicate that the lack of RelB is, in part, compensated by other p50 containing complexes and that the `` classical '' p50-RelA-NF-kappaB activity is not required for the development of the inflammatory phenotype