NF-kB Pathway Assay (CAT#: STEM-MB-0345-WXH)

NF-κB activation occurs via two major signaling pathways: the canonical and the non-canonical NF-κB signaling pathways.
• The canonical NF-κB pathway is triggered by signals from a large variety of immune receptors, such as TNFR, TLR, and IL-1R, which activate TAK1. TAK1 then activates IκB kinase (IKK) complex, composed of catalytic (IKKα and IKKβ) and regulatory (NEMO) subunits, via phosphorylation of IKKβ. Upon stimulation, the IKK complex, largely through IKKβ, phosphorylates members of the inhibitor of κB (IκB) family. Upon phosphorylation by IKK, IκBα and p105 are degradated in the proteasome, resulting in the nuclear translocation of canonical NF-κB family members, which bind to specific DNA elements, in the form of various dimeric complexes.
• The non-canonical NF-κB pathway is induced by certain TNF superfamily members, such as CD40L, BAFF and lymphotoxin-β (LT-β), which stimulates the recruitment of TRAF2, TRAF3, cIAP1/2 to the receptor complex. Activated cIAP mediates K48 ubiquitylation and proteasomal degradation of TRAF3, resulting in stabilization and accumulation of the NFκB-inducing kinase (NIK). NIK phosphorylates and activates IKKα, which in turn phosphorylates p100, triggering p100 processing, and leading to the generation of p52 and the nuclear translocation of p52 and RELB.

To study the effects of drugs or therapies on NF-κB signaling pathways
To study the effect of each virus on NF-κB signaling pathway
To study the regulation mechanism of NF-κB signaling pathway in disease

• Luminex Multiplex Assay
• Enzyme-linked immunosorbent assay (ELISA)
• Flow cytometry (FACS analysis) technology

Detectable targets: LYN, SYK, BLK, MYD88, RIPK1, TRADD, TRAF2, TRAF5, RNF135, TRIM25, TIRAP, TRAM, TRIF, TRAF6, RIP1, TRAF3, clAP1, clAP2, NIK, TBK1, MKK3, NFκB, MKK4, MKK6, MKK7, IPS1, IRAK1, IRAK4, BLNK, BTK, DAG, PKC, ELKs, REL, CK2, ATM, IKK-α, NEMO, PIDD, p50, RIP1, PARP1, SUMO, RELA, lkBa, IRF7, Tak1, IRF3, BCL-10, p38, p52, RELB, TBK1, PKC, IKK-β