{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNF‑κB2 is a multifaceted regulatory molecule that functions both as a precursor protein (p100) and as an active transcription factor (p52) in the noncanonical NF‑κB signaling pathway. In its latent p100 state, NF‑κB2 sequesters other NF‑κB subunits into high‐molecular‐weight complexes, thereby acting as an inhibitor. Upon appropriate stimulation, processing of p100 into p52 occurs through a tightly controlled mechanism that involves the inducible kinases NIK and IKKα, site‐specific phosphorylation, recruitment of the SCFβ‑TrCP E3 ubiquitin ligase, and subsequent proteasomal degradation of the C‑terminal inhibitory domain. Structural studies further reveal that p100 interacts with other NF‑κB members via its ankyrin repeats and undergoes conformational changes essential for its dual roles in inhibition and transcriptional activation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the immune system, NF‑κB2 is pivotal in orchestrating B cell development, lymphoid organogenesis, and the regulation of inflammatory responses. Mutations in NFKB2 that impair p100 processing have been causally linked to primary immunodeficiency disorders such as common variable immunodeficiency (CVID) and DAVID syndrome, often presenting with hypogammaglobulinemia, autoimmunity, and endocrine abnormalities. Moreover, NF‑κB2 activity is modulated by external signals—ranging from lymphotoxin‐β receptor and CD40 engagement to viral proteins and pathogen‐derived stimuli—that influence its processing and nuclear translocation, thereby fine‐tuning immune responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, NF‑κB2 plays a dual role by promoting survival, proliferation, and resistance to therapy while also participating in oncogenic transformation. The active p52 subunit engages in transcriptional regulation of cell cycle genes, antiapoptotic factors, and mediators that enable chemoresistance and hormone receptor activation. In several tumor types—including prostate, breast, lung, and hematologic malignancies—viral oncoproteins (such as EBV LMP1 and HTLV‑1 Tax1), mutant p53, and Stat3 converge on the noncanonical NF‑κB2 signaling axis to drive oncogenesis through mechanisms such as androgen receptor splice variant formation and repressive chromatin remodeling. These insights underscore the importance of NF‑κB2 as a therapeutic target, while also highlighting the challenge of achieving pathway‐specific interventions that do not compromise normal immune function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Abraham Fong, Shao-Cong Sun "}, {"type": "b", "children": [{"type": "t", "text": "Genetic evidence for the essential role of beta-transducin repeat-containing protein in the inducible processing of NF-kappa B2/p100."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.C200151200"}], "href": "https://doi.org/10.1074/jbc.C200151200"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "11994270"}], "href": "https://pubmed.ncbi.nlm.nih.gov/11994270"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Estefania Claudio, Keith Brown, Sun Park, et al. 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