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MIPEP — RELA

Text-mined interactions from Literome

Dejardin et al., Immunity 2002 : IKKbeta dependent activation of canonical NF-kappaB is required for the expression but not processing of p100 and for the expression of proinflammatory molecules including VCAM-1, MIP-1beta , and MIP-2 in response to LTbetaR ligation
Guo et al., J Neurochem 2003 : These data suggest that NF-kappaB is at least partially involved in the IL-1beta mediated action on MIP-1alpha and -1beta in NT2-N cells
Kwon et al., Biochem Biophys Res Commun 2003 : We also provided evidence that NF-kappaB and c-Jun contributes to the expression of MIP-2 gene in response to CpG-ODN, since ectopical expression of NF-kappaB and c-Jun in RAW 246.7 cells leads to dramatically increase the ability of CpG-ODN 1826 ( S ) in MIP-2 promoter activity
Kim et al., Mol Immunol 2003 : Inhibition of NF-kappaB nuclear localization by co-expression of a mutant IkappaBalpha protein ( IkappaBalpha super repressor, IkappaBalphaSR ) blocked LPS induced transcription from a MIP-2 promoter-reporter construct, showing that NF-kappaB activation is required for MIP-2 gene expression in the LPS signaling pathway
Gregory et al., Eur J Immunol 2008 : Importantly, induction of chemokine gene expression ( MIP-2/CXCL2 , MCP-1/CCL2, MIP-1alpha/CCL3, MIP-1beta/CCL4 ) by Leishmania is NF-kappaB dependent , which implies that p35 RelA/p50 dimers are able to activate transcription, despite the absence of a recognized transcriptional transactivation domain