RelBp52

RelBp52 is the transcription factor complex formed by RelB and the p52 subunit, both members of the NF-κB family. As a noncanonical NF-κB dimer, RelBp52 participates in signaling routes that regulate immune system development and function, particularly in lymphoid tissues and antigen-presenting cells.

Activation and mechanism

RelBp52 activity is driven by the noncanonical NF-κB pathway. In this pathway, the precursor p100 is processed to p52 through the action of NF-κB-inducing kinase (NIK) and IκB kinase α (IKKα). The resulting RelB:p52 dimer translocates to the nucleus, where it binds κB sites in DNA to regulate gene transcription. This process is distinct from the canonical NF-κB pathway and relies on the accumulation of p52 and RelB rather than p50-containing dimers.

DNA binding and target genes

RelBp52 binds to κB-responsive elements with specificity that supports regulation of genes involved in lymphoid organogenesis, B-cell development, dendritic cell maturation, and various cytokine and chemokine pathways. Target genes include those governing cell survival, differentiation, and immune signaling, contributing to properly organized immune responses.

Regulation and biological significance

RelBp52 activity is controlled by the balance of p100/p52 processing, RelB availability, and interactions with co-regulators and IκB family members. Dysregulation of RelBp52 signaling can impact lymphoid tissue development and immune cell function, and abnormal NF-κB signaling in general is linked to immune disorders and certain cancers. Because RelBp52 coordinates essential immune processes, it is a point of interest for therapeutic strategies aiming to modulate noncanonical NF-κB signaling.

See also

NF-κB signaling, RelB, NFKB2, p100/p52, IKKα, NIK.