James E. Vince

Walter and Eliza Hall Institute of Medical Research
Australia

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name Citations Publications World Ranking National Ranking

Biology and Biochemistry D-index 40 Citations 8,964 83 World Ranking 17783 National Ranking 525

Overview

What are the main themes of his work throughout his whole career to date

Cell biology is often connected to Effector in his work. His Cell biology research extends to Effector, which is thematically connected. His Biochemistry study frequently links to adjacent areas such as Biogenesis. By researching both Biogenesis and Gene, he produces research that crosses academic boundaries. In his works, James E Vince performs multidisciplinary study on Gene and Gene expression. His Genetics research extends to the thematically linked field of Gene expression. As part of his studies on Genetics, he often connects relevant areas like Cancer cell. In his articles, he combines various disciplines, including Cancer cell and Apoptosis. He conducted interdisciplinary study in his works that combined Apoptosis and Inhibitor of apoptosis.

James E Vince most often published in these fields:

Cell biology (100.00%)
Biochemistry (75.00%)
Immunology (50.00%)

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.

Best Publications

IAP Antagonists Target cIAP1 to Induce TNFα-Dependent Apoptosis

James E. Vince;W. Wei-Lynn Wong;Nufail Khan;Rebecca Feltham.
Cell (2007)

1168 Citations

Recruitment of the Linear Ubiquitin Chain Assembly Complex Stabilizes the TNF-R1 Signaling Complex and Is Required for TNF-Mediated Gene Induction

Tobias L. Haas;Christoph H. Emmerich;Christoph H. Emmerich;Bjã¶rn Gerlach;Bjã¶rn Gerlach;Anna C. Schmukle.
Molecular Cell (2009)

735 Citations

RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis.

James A Rickard;James A Rickard;Joanne A O'Donnell;Joanne A O'Donnell;Joseph M Evans;Joseph M Evans;Najoua Lalaoui;Najoua Lalaoui.
Cell (2014)

508 Citations

Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation.

James E. Vince;W. Wei Lynn Wong;W. Wei Lynn Wong;Ian Gentle;Kate E. Lawlor;Kate E. Lawlor.
Immunity (2012)

486 Citations

RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL

Kate E. Lawlor;Nufail Khan;Alison Mildenhall;Motti Gerlic.
Nature Communications (2015)

475 Citations

AIM2 and NLRP3 inflammasomes activate both apoptotic and pyroptotic death pathways via ASC

V Sagulenko;S J Thygesen;D P Sester;A Idris.
Cell Death & Differentiation (2013)

427 Citations

Pyroptosis versus necroptosis: similarities, differences, and crosstalk

Daniel Frank;Daniel Frank;James E. Vince;James E. Vince.
Cell Death & Differentiation (2019)

418 Citations

The NLRP3 inflammasome in health and disease: the good, the bad and the ugly

P Menu;J E Vince.
Clinical and Experimental Immunology (2011)

350 Citations

Active MLKL triggers the NLRP3 inflammasome in a cell-intrinsic manner.

Stephanie A. Conos;Stephanie A. Conos;Kaiwen W Chen;Dominic De Nardo;Dominic De Nardo;Hideki Hara.
Proceedings of the National Academy of Sciences of the United States of America (2017)

269 Citations

TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1–TRAF2 complex to sensitize tumor cells to TNFα

James E. Vince;Diep Chau;Bernard Callus;W. Wei-Lynn Wong.
Journal of Cell Biology (2008)

256 Citations

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