c-IAP1 and c-IAP2 Are Critical Mediators of Tumor Necrosis Factor α (TNFα)-induced NF-κB ActivationEugene Varfolomeev, Domagoj Vucic|Journal of Biological Chemistry|2008Cited by 536
RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injuryKim Newton, Domagoj Vucic|Cell Death and Differentiation|2016Cited by 439
The Balance of TNF Mediated Pathways Regulates Inflammatory Cell Death Signaling in Healthy and Diseased TissuesJoshua D. Webster, Domagoj Vucic|Frontiers in Cell and Developmental Biology|2020Cited by 359
c‐IAP1 and UbcH5 promote K11‐linked polyubiquitination of RIP1 in TNF signallingJasmin N. Dynek, Domagoj Vucic|The EMBO Journal|2010Cited by 338
RIP1 inhibition blocks inflammatory diseases but not tumor growth or metastasesSnahel Patel, Domagoj Vucic|Cell Death and Differentiation|2019Cited by 145