Overview:

Rel B is part of the NFκB complex and forms heterodimeric complexes with p50 (NFKB1) and p52 (NFKB2) (1). The homodimeric complexes of Rel B alone do not show DNA-binding activity. IHC analysis has shown that Rel B expression correlated with dendritic cell activation. NFκB-inducing kinase NIK is required for osteoclastogenesis in response to pathologic stimuli and overexpression of Rel B rescues differentiation of mouse NIK -/- osteoclast precursors. Rel B is required for RANKL-induced osteoclastogenesis in vitro and for TNF -induced bone resorption in vivo. This indicates that the alternative NFκB pathway, via Rel B, plays an essential and unique role in RANKL signaling toward osteoclast development (2).

Gene Aliases:

IREL, I-REL

Genbank Number:

NM_006509

References:

1. Bours, V. et al: Human RelB (I-Rel) functions as a kappa-B site-dependent transactivating member of the family of Rel-related proteins. Oncogene 9: 1699-1702, 1994.

2. Vaira, S. Et al: RelB is the NF-kappa-B subunit downstream of NIK responsible for osteoclast differentiation. Proc. Nat. Acad. Sci. 105: 3897-3902, 2008