Structural basis of IAP recognition by Smac/DIABLO

By Geng Wu, J. Chai, T. L. Suber, Jia-Wei Wu, Chunying Du, Xiaodong Wang, Yigong Shi. Nature, 2000

880 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/48268e6b16f791e8ce95bf6cf317121750f482af

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Citations in the corpus

Structural basis for the inhibition of caspase-3 by XIAP. (2001, neutral): “In modeling the N terminus (Liu et al., 2000; Wu et al., 2000).”
Toxic proteins released from mitochondria in cell death (2004, background): “Structural analysis has revealed that the four N-terminal amino acids of Smac tether to a hydrophobic surface groove on the BIR3 domain of XIAP (Liu et al., 2000; Wu et al., 2000).”
Autocrine TNFalpha signaling renders human cancer cells susceptible to Smac-mimetic-induced apoptosis. (2007, background): “Interestingly, although there was no significant difference in XIAP/TRAF1/TRAF2 pulled down from sensitive (HCC44 and HCC461) or nonsensitive (HCC827 and H2009) cell extracts, there seemed to be more cIAPs from the sensitive cells pulled down by the biotinylated Smac mimetic.”
Molecular mechanisms of caspase regulation during apoptosis (2004, background): “Due to the cleavage of the mitochondria-targeting sequence, the mature SMAC/DIABLO protein contains a tetrapeptide at its N terminus — Ala-Val-Pro-Ile — which binds to the conserved surface groove on the BIR3 domain of XIAP (Ref”
Mechanisms of caspase activation and inhibition during apoptosis. (2002, background): “In protein (Wu et al., 2000) or a nine residue Smac peptide (Liu et al., 2000).”
Mechanism of XIAP-mediated inhibition of caspase-9. (2003, background): “Strikingly, IAP binding motif located at the N terminus of the mature the surface of caspase-9 that interacts with BIR3 also protein (Liu et al., 2000; Shi, 2002a; Wu et al., 2000).”
A Comprehensive Model for the Cellular Uptake of Cationic Cell‐penetrating Peptides (2007, methodology): “Pretreatment of cells with the Smac–R9 conjugate potentiated the induction of caspase-3 activation in a concentration-dependent manner byup to 100% (Figure 12B).”
Targeting IAP proteins for therapeutic intervention in cancer (2012, background): “SMAC promotes caspase activation and apoptosis by binding to several IAP proteins, including XIAP, c-IAP1 and c-IAP2, via its amino-terminal amino acid residues (Ala-Val-Pro-Ile) that are highly conserved through evolutio”
Regulation of tumour necrosis factor signalling: live or let die (2015, background): “In an experimental setting, SMAC mimetics bind to the baculovirus IAP repeat domain of cIAP1 and cIAP2 and thereby turn on their E3 ubiquitin ligase activity 73 .”