Gene interactions and pathways from curated databases and text-mining

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REL — RELA

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

Silverman et al., Genes Dev 2000 : Remarkably, this Drosophila IkappaB kinase complex is not required for the activation of the Rel proteins Dif and Dorsal through the Toll signaling pathway, which is essential for antifungal immunity and dorsoventral patterning during early development ... Thus, a yet to be identified IkappaB kinase complex must be required for Rel protein activation via the Toll signaling pathway
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
Szabo et al., Frontiers in bioscience : a journal and virtual library 2002 : Activation of NF-kappa B , however, is regulated at multiple levels including I-kappa B degradation, nuclear translocation, and by interaction of NF-kappa B/Rel with other transcription factors
Antonsson et al., Mol Cell Biol 2003 : Our results suggest that CaM binds c-Rel and RelA after their release from I kappa B and can inhibit nuclear import of c-Rel while letting RelA translocate to the nucleus and act on its target genes
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
Ravi et al., Drug Resist Updat 2004 (Neoplasms) : NF-kappaB may be inhibited by targeting either the apical signaling proteins responsible for its activation in specific types of cancer, the downstream kinases ( IkappaB kinase and casein kinase 2 ) at which NF-kappaB activating signaling pathways converge, the proteasome mediated degradation of the inhibitor of kappaB ( IkappaB ) proteins, or the transcriptional activity of Rel proteins
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
Thornburg et al., Oncogene 2006 (Lymphoma) : The LMP1 mediated activation of NF-kappaB may contribute to the specific activation of c-Rel and lead to the increased development of lymphoma in the LMP1 transgenic mice
Ballard et al., Cell 1990 : v-Rel , but not nontransforming v-Rel mutants, binds to the kappa B enhancer and inhibits NF-kappa B-activated transcription from the IL-2 receptor alpha promoter and HIV-1 LTR