Domagoj Vucic

Principal Scientist, Early Discovery Biochemistry

Postdoc Mentor

"Blocking cell death to prevent tissue damage"

Years at Genentech

Publications

My laboratory studies the biological role of regulators of cell death and signaling pathways (e.g. ubiquitination-mediated regulation of NF-κB pathways), and their involvement in cellular processes triggered by TNF family ligands and other pro-inflammatory stimuli. As part of this effort we are studying how ubiquitination, phosphorylation and other post-translational modifications affect functional properties of mediators of various signaling pathways including apoptosis, necroptosis and NF-κB activation. To this end we are exploring the therapeutic potential of targeting select kinases and ubiquitin ligases for the treatment of uncontrolled inflammatory responses and/or enhancement of the survival of damaged tissues.

Postdoctoral Mentor

I cherish the opportunity to coach young scientists and guide their energy and enthusiasm for science into well organized thoughts and carefully planned experiments that will lay the foundation for their future scientific careers.

Featured Publication

RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury.

Cell Death Differ. 2016 Sep 1;23(9):1565-76.

Newton K, Dugger DL, Maltzman A, Greve JM, Hedehus M, Martin-McNulty B, Carano RA, Cao TC, van Bruggen N, Bernstein L, Lee WP, Wu X, DeVoss J, Zhang J, Jeet S, Peng I, McKenzie BS, Roose-Girma M, Caplazi P, Diehl L, Webster JD, Vucic D.

View Abstract

We are investigating the physiological role of RIP family of kinases and inhibitors of apoptosis (IAP) proteins in modulation of immune responses. IAP proteins physically interact with a variety of mediators of inflammation and cell death and they regulate these signaling pathways by promoting ubiquitination of RIP1 and RIP2 kinases. In collaboration with other groups at Genentech we are developing genetic models and small-molecule compounds to evaluate the physiological contribution and therapeutic potential of distinct IAP proteins and RIP kinases in diseases impacted by inflammatory and cell death.

The kinase TPL2 activates ERK and p38 signaling to promote neutrophilic inflammation

Science Signaling, ISSN: 19450877

Kate Senger; Victoria Pham; Eugene Varfolomeev; Jason Hackney; Alex Corzo; Jenna Collier; Vivian W. C. Lau; Zhiyu Huang; Kajal Hamidzhadeh; Patrick Caplazi; Ivan Peng; Francesca Setiadi; Ross Francis; Andres Paler Martinez; Youngsu Kwon; Vladimir Ramirez Carrozzi; Yonglian Sun; Patricia Grigg; Meron Roose-Girma; Surinder Jeet; Kai Barck; Anna Pham; Ota; Connie Ha; Jeremy Stinson; Joe Guillory; Lucinda Tam; Zora Modrusan; Claire Emson; Brent McKenzie; Michael Townsend; Rick Carano; Soren Warming; Domagoj Vucic; Jason De Voss; Wyne Lee; Jennie Lill; Ali Zarrin

The kinase TPL2 activates ERK and p38 signaling to promote neutrophilic inflammation

Science Signaling, ISSN: 19379145

Kate Senger; Victoria Pham; Eugene Varfolomeev; Jason Hackney; Alex Corzo; Jenna Collier; Vivian W. C. Lau; Zhiyu Huang; Kajal Hamidzhadeh; Patrick Caplazi; Ivan Peng; Francesca Setiadi; Ross Francis; Andres Paler Martinez; Youngsu Kwon; Vladimir Ramirez Carrozzi; Yonglian Sun; Patricia Grigg; Meron Roose-Girma; Surinder Jeet; Kai Barck; Anna Pham; Neko Ota; Connie Ha; Jeremy Stinson; Joe Guillory; Lucinda Tam; Zora Modrusan; Claire Emson; Brent McKenzie; Michael Townsend; Rick Carano; Soren Warming; Domagoj Vucic; Jason De Voss; Wyne Lee; Jennie Lill; Ali Zarrin

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Domagoj Vucic

Principal Scientist, Early Discovery Biochemistry

Featured Publication

RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury.