NF-κB Signaling Pathway Research Reagents

NF-κB p65 (RELA) — The major transactivation subunit of canonical NF-κB signaling. p65 nuclear translocation is the standard readout for NF-κB pathway activation in immunofluorescence and Western blot assays. Phospho-p65 (Ser536) is a widely used activation marker.
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NF-κB1 (p105/p50) — p105 is the precursor that is processed to p50 via the proteasome. p50/p65 heterodimers are the most abundant NF-κB complex. p50 homodimers can act as transcriptional repressors.
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NF-κB2 (p100/p52) — Central to the non-canonical (alternative) NF-κB pathway. p100 processing to p52 is triggered by NIK and is critical for lymphoid organ development, B cell survival, and bone metabolism.
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IKKα (CHUK) — Catalytic subunit of the IKK complex with a primary role in the non-canonical NF-κB pathway. Also contributes to canonical signaling and epigenetic regulation of NF-κB target genes.
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IKKβ (IKBKB) — The dominant catalytic subunit for canonical NF-κB activation. IKKβ directly phosphorylates IκBα at Ser32/36, marking it for ubiquitination and proteasomal degradation. A major drug target in inflammatory disease.
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IκBα (NFKBIA) — The primary cytoplasmic inhibitor that sequesters NF-κB dimers. Stimulus-induced IκBα phosphorylation and degradation is the gating step for NF-κB nuclear entry. IκBα degradation kinetics are a standard functional readout in pathway studies.
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TRAF6 — E3 ubiquitin ligase and critical signaling adaptor downstream of IL-1R/TLR and RANK receptor families. TRAF6 mediates K63-linked polyubiquitination to activate the TAK1-IKK axis. Essential for innate immunity, osteoclastogenesis, and lymph node organogenesis.
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TRAF2 — Adaptor protein downstream of TNF receptor superfamily members. TRAF2 recruits cIAP1/2 E3 ligases to activate canonical NF-κB signaling and suppress TNF-induced apoptosis. Also regulates JNK and non-canonical NF-κB pathways.
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4. Sun SC. The non-canonical NF-κB pathway in immunity and inflammation. Nat Rev Immunol. 2017;17(9):545-558. DOI