EFkB

EFkB is not a widely established term in molecular biology. In many contexts it appears as a typographical variant of NF-κB, a central transcription factor in immune and inflammatory signaling, or as a hypothetical or fictional label. There is no officially recognized protein or gene universally named EFkB in major databases, so the term is typically considered a misspelling, an informal shorthand, or a placeholder rather than a distinct molecular entity.

If EFkB is intended to refer to NF-κB, the acronym would point to a family of transcription factors that regulate gene expression in response to stress, cytokines, free radicals, and microbial products. NF-κB typically forms dimers from Rel family proteins, including p65 (RelA), RelB, c-Rel, p50 (NF-κB1), and p52 (NF-κB2). In resting cells, these dimers are held in the cytoplasm by inhibitors known as IκBs. Stimulatory signals activate IκB kinases (IKKs), leading to IκB phosphorylation and degradation, allowing NF-κB to enter the nucleus and bind κB sites to control target genes such as cytokines, chemokines, adhesion molecules, and anti-apoptotic proteins.

Regulation of NF-κB involves canonical and non-canonical pathways, post-translational modifications, and cross-talk with other signaling networks. Aberrant NF-κB activity is associated with inflammatory diseases, autoimmune conditions, cancer, and other disorders.

In scientific literature and databases, researchers should use the official NF-κB nomenclature and subunit symbols, such as NFKB1, NFKB2, RELA, RELB, and REL, and refer to IκB and IKK as key regulators. If EFkB appears in a source, it is advisable to verify whether it is a misprint or a context-specific, non-standard usage.