High impact information on RELB

• Transfection experiments demonstrate that I-Rel suppresses NF-kappa B-induced transcription, probably through its association with p50 [1].
• The transcription factor RelB is required for proper development and function of dendritic cells (DCs), and its expression is upregulated early during differentiation from a variety of progenitors [2].
• Here we demonstrate that the nuclear factor-kappaB (NF-kappaB) transcription factor RelB regulates the generation of monocytic CD14(+)CD11b(+) precursors of interstitial DCs from human hematopoietic progenitors [3].
• On the other hand, the I-Rel protein, the presumed human homolog of RelB, was proposed to be an inhibitor whose presence in dimeric complexes interfered with their kappa B binding and therefore interfered also with transactivation [4].
• DETA-NONOate evoked a wave of expression changes (maximum at 4 h), with a remarkable downregulation of the transcription factors MSX1, RELB, and Egr-1 [5].

Biological context of RELB

• We demonstrate that human RelB (I-Rel) forms with p50 and p52 (p50B) kappa B-binding heterodimeric complexes which potently transactivate kappa B-dependent constructs in transfection studies [4].
• A critical role of NF-kappaB in promoting cell survival in IFN-alpha-resistant cells is indicated by the upregulation of RELB and LTB [6].

Other interactions of RELB

• A relatively high number of genes involved in innate and inflammatory host immune responses, including interleukin-8, interleukin-6, NF-kappaB(2), RELB and fos, were induced [7].
• Triggering of this receptor induces a unique signalling cascade leading to the activation of the transcription factor RelB through activation of NF-kappa B inducing kinase [8].

References