Death Receptor Pathway Assay (CAT#: STEM-MB-0346-WXH)

Death receptor ligands initiate signal transduction through receptor oligomerization, which leads to the recruitment of specific adaptor proteins and the activation of the caspase cascade. The binding of FasL induces the trimerization of Fas, thereby recruiting priming caspase-8 through the adaptor protein FADD. Then, caspase-8 is oligomerized and activated by autocatalysis. Activated caspase-8 can induce apoptosis through two parallel cascades: it can either directly cleave and activate caspase-3, or cleave the pro-apoptotic protein Bid of the Bcl-2 family. The truncated Bid (tBid) translocates into the mitochondria and induces the release of cytochrome C, thereby activating caspase-9 and -3. TNF-α and DR-3L can transmit pro-apoptotic or anti-apoptotic signals. TNFαR and DR3 promote cell apoptosis through the adaptor protein TRADD/FADD and activation of caspase-8. The interaction between TNF-α and TNFαR can activate the NF-κB pathway through NIK/IKK. The activation of NF-κB induces the expression of pro-survival genes, including Bcl-2 and FLIP, the latter can directly inhibit the activation of caspase-8. FasL and TNF-α can also activate JNK through ASK1/MKK7. Activation of JNK inhibits Bcl-2 through phosphorylation. In the absence of caspase activation, the stimulation of death receptors can lead to the activation of another programmed cell death pathway through the formation of complex IIb, which is called necroptosis.

To study the effect of each virus on death receptor signaling pathway
To study the regulation mechanism of death receptor signal pathway in disease
To study the effects of drugs or therapies on death receptor signaling pathways

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

Detectable targets: MKK1, Daxx, FADD, TRADD, TRAF1, TRAF2, RIP, Casp-8, JNK, Casp-10, CYLD, clAP1, clAP2, BID, tBID, Bcl-2, MKK1, Casp-9, XIAP, Casp-6, Casp-3, NFκB, Casp-7, , TRAF1, GAS, IRF9, Smac, IkB, RelB, TRAF2, Lamin, A, Actin, GAS2, ROCK1, DFF45, TRAF3, IKK-α, Acinus, PARP, p52, Cyto, c, Apaf1, IKK-β, DFF40, NIK, p65