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Fig. 1 | BMC Molecular and Cell Biology

Fig. 1

From: Identification of potential binding pocket on viral oncoprotein HPV16 E6: a promising anti-cancer target for small molecule drug discovery

Fig. 1

Schematic representation of extrinsic apoptotic pathway and HPV E6 blockade of FADD mediated apoptosis. Under normal conditions, binding of death ligands such as FasL, TNF, TRAIL to their receptors e.g., Fas, TNF-R, TRAIL-R initiates an extrinsic apoptotic pathway. This leads to the association of adaptor molecules such as FADD, TRADD to the death receptor forming a death inducing signaling complex (DISC), which activates procaspase 8. Activated procaspase 8 releases active cysteine-aspartic proteases that enable caspase 8 to cleave and activate effector caspases 3 and 7. However, in the case of HPV E6 oncoprotein expressed cells this sequence cannot occur. HPV E6 binds to FADD blocking procaspase 8 activation and subsequent actions. This binding also leads to the degradation of FADD. Both of these events prevent apoptosis and cells become resistant to cell death induced by TNF and TRAIL

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