DNA-PK Signaling Pathway Assay (CAT#: STEM-MB-0310-WXH)

After induction of the DNA-strand break, the broken DNA is quickly recognized and bound by the Ku70/80 heterodimer. The heterodimer forms a ring-like protein complex at the lesion site, which stabilizes the broken DNA double strands. At the same time, the Ku heterodimer recruits related processing proteins. The Ku heterodimer also serves to maintain the stabilization of this NHEJ complex at the DNA damage site. Then the NHEJ complex bridges the DNA ends and further promotes the end stability. The interaction of DNA-PKcs and Ku heterodimer leads to translocation of the Ku heterodimer inward on the dsDNA strand and ultimately results in activation of the DNA-PKcs kinase activity. After the DNA ligase IV-X-ray cross complementing protein 4 (XRCC4) complex ligates the broken ends with the assistance of the XRCC4-like factor (XLF), NHEJ complex leaves the DNA, which marks the completion of the NHEJ.

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

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

Detectable targets: ATR, TopBP1, PP6, H2AK, CHK2, Bad, Chk2, p73, PIDD, MYD88, Rac1, TLR4, Chk1, p63, TRAF-2, FADD, APAF-1, BID, BRCA1, IRF7, Mda-5, NFκB, RIG-1, TRAF3, WRN, IRF9, MEKK1, p38, RIP1, TRAF5, Histone-H3, IRF5, MEK3, p38MAPK, SH2, TRAF6, IKK-α, IRS1, MEK6, p50, SLP76, TRAM, IPS-1, ISGF3, MSK2, PI3K, TBK1, Vav, IRAK1, ISRE, mTOR, PKR, TLR3