His primary areas of study are Cell biology, Inhibitor of apoptosis, Programmed cell death, XIAP and Apoptosis. His Cell biology study incorporates themes from Inflammasome and NLRC4. The concepts of his Inhibitor of apoptosis study are interwoven with issues in Ubiquitin, Ubiquitin ligase and Ubiquitin-conjugating enzyme.
His Programmed cell death study combines topics in areas such as Tumor necrosis factor alpha and Kinase activity. His Tumor necrosis factor alpha study combines topics from a wide range of disciplines, such as Kinase and RIPK1, Necroptosis. His research investigates the connection between Apoptosis and topics such as Cancer cell that intersect with issues in Caspase, Activator, Proteases and Targeted therapy.
The scientist’s investigation covers issues in Cell biology, Inhibitor of apoptosis, Apoptosis, Programmed cell death and XIAP. Domagoj Vucic interconnects Ubiquitin and Ubiquitin ligase in the investigation of issues within Cell biology. His study looks at the relationship between Inhibitor of apoptosis and fields such as Cancer cell, as well as how they intersect with chemical problems.
The study incorporates disciplines such as Cancer, Cancer research and Immunology in addition to Apoptosis. His Programmed cell death research is multidisciplinary, relying on both Tumor necrosis factor alpha, Proinflammatory cytokine and Drug discovery. His work carried out in the field of XIAP brings together such families of science as Baculoviral IAP repeat-containing protein 3, Plasma protein binding, Antagonist, Activator and Cellular homeostasis.
Domagoj Vucic focuses on Programmed cell death, Kinase, RIPK1, Kinase activity and Inflammation. As part of his studies on Programmed cell death, he often connects relevant areas like Cell biology. The study incorporates disciplines such as Ubiquitin and Epigenetics in addition to Cell biology.
His studies examine the connections between Kinase and genetics, as well as such issues in Necroptosis, with regards to Cancer research, Caspase, Neurodegeneration and Protein kinase A. Particularly relevant to Inhibitor of apoptosis is his body of work in Apoptosis. His Inhibitor of apoptosis research incorporates themes from Proinflammatory cytokine, XIAP, Chemokine and Caspase 8.
His main research concerns Kinase, Inflammation, Cancer research, Necroptosis and Kinase activity. His study in the field of Kinase inhibition also crosses realms of IRAK4. The concepts of his Inflammation study are interwoven with issues in Bruton's tyrosine kinase and Bioinformatics.
His Cancer research research is multidisciplinary, incorporating perspectives in RIPK1, Immune system, Caspase, Programmed cell death and Tumor progression. His Necroptosis research integrates issues from Signal transduction and Arthritis.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf.
Sanjeev Mariathasan;Kim Newton;Denise M. Monack;Domagoj Vucic.
IAP antagonists induce autoubiquitination of c-IAPs, NF-kappaB activation, and TNFalpha-dependent apoptosis.
Eugene Varfolomeev;John W. Blankenship;Sarah M. Wayson;Anna V. Fedorova.
Targeting IAP proteins for therapeutic intervention in cancer.
Simone Fulda;Domagoj Vucic.
Nature Reviews Drug Discovery (2012)
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
Lorenzo Galluzzi;Ilio Vitale;Stuart A. Aaronson;John M. Abrams.
Ubiquitination in disease pathogenesis and treatment
Doris Popovic;Domagoj Vucic;Ivan Dikic.
Nature Medicine (2014)
ML-IAP, a novel inhibitor of apoptosis that is preferentially expressed in human melanomas.
Domagoj Vucic;Henning R. Stennicke;Maria Teresa Pisabarro;Guy S. Salvesen.
Current Biology (2000)
c-IAP1 and c-IAP2 Are Critical Mediators of Tumor Necrosis Factor α (TNFα)-induced NF-κB Activation
Eugene Varfolomeev;Tatiana Goncharov;Anna V. Fedorova;Jasmin N. Dynek.
Journal of Biological Chemistry (2008)
Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis.
Kim Newton;Debra L. Dugger;Katherine E. Wickliffe;Neeraj Kapoor.
Ubiquitylation in apoptosis: a post-translational modification at the edge of life and death
Domagoj Vucic;Vishva M. Dixit;Ingrid E. Wertz.
Nature Reviews Molecular Cell Biology (2011)
RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury.
K Newton;D L Dugger;A Maltzman;J M Greve.
Cell Death & Differentiation (2016)
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