Genentech: Kim Newton | Senior Scientist, Physiological Chemistry

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Scientists / Our Scientists

Years at Genentech

Publications

Awards & Honors

I joined Genentech in 2001 as a postdoc after completing my PhD in the cell death lab of Andreas Strasser at the Walter & Eliza Hall Institute in Australia. As a postdoc with Vishva Dixit, I worked on several projects including the role of the adaptor protein CARMA1/CARD11 in lymphocyte development and activation, the effect of TNF family ligands EDA-A1 and EDA-A2 on hair, sweat gland and muscle homeostasis, and the characterization of a kinase called RIPK3, which turned out to be a key effector of a regulated form of necrotic cell death termed necroptosis. These diverse projects were developed in collaboration with several departments and I saw first hand how much can be achieved when experts across disciplines pull together. Enthusiastic, talented colleagues combined with exciting, medically relevant science made staying on as a scientist an easy decision.

The current mission of my group is to decipher the signaling mechanisms unleashing proinflammatory cell death programs that may exacerbate a range of inflammatory diseases. Our goal is to unveil novel therapeutics targets with the potential to benefit patients.

Featured Publication

RIPK1 inhibits ZBP1-driven necroptosis during development.

Nature. 2016 Dec 1;540(7631):129-133.

Newton K, Wickliffe KE, Maltzman A, Dugger DL, Strasser A, Pham VC, Lill JR, Roose-Girma M, Warming S, Solon M, Ngu H, Webster JD, Dixit VM.

View Abstract

Inflammation is a driving factor in many chronic diseases. My group studies the contribution of cell death to inflammation because dying cells can release molecules that activate innate immune cells to produce an inflammatory response. Recent work has focused on the kinases RIPK1 and RIPK3 because of their contribution to proinflammatory cell death. We are using genetic and biochemical approaches to understand how, when and where these kinases get activated, as well as the signaling mechanisms that normally hold these kinases in check.

Ubiquitin ligase COP1 coordinates transcriptional programs that control cell type specification in the developing mouse brain

Proceedings of the National Academy of Sciences of the United States of America,

Kim Newton; Debbie Dugger; Arundhati Sengupta Ghosh; Ronald E. Ferrando; Felix Chu; Janet Tao; Wendy Lam; Susan Haller; Sara Chan; Susan Sa; Debra Dunlap; Jeff Eastham; Hai Ngu; Jeffrey Hung; Dorothy French; Webster; Brad Bolon; Jinfeng Liu; Rohit Reja; Sarah Kummerfeld; Ying-Jiun Chen; Zora Modrusan; Joe Lewcock; Vishva Dixit

Kinase domain dimerization drives RIPK3-dependent necroptosis

Science Signaling, ISSN: 19450877

Saravanan Raju; Dan Whalen; Meron Mengistu; Carter J. Swanson; John G. Quinn; Susan Taylor; Webster; Kim Newton; Andrey Shaw

OTULIN limits cell death and inflammation by deubiquitinating LUBAC

Nature, ISSN: 14764687 00280836

Klaus Heger; Kate Wickliffe; Ada Ndoja; Juan Zhang; Aditya Murthy; Debbie Dugger; Maltzman; Felipe de Sousa e Melo; Jeffrey Hung; Yi Zeng; Erik Verschueren; Don Kirkpatrick; Domagoj Vucic; Wyne Lee; Meron Roose-Girma; Robert J (Research) Newman; Soren Warming; Yi-Chun Hsiao; László Kömüves; Webster; Kim Newton; Vishva Dixit

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Kim Newton

Senior Scientist, Physiological Chemistry

Featured Publication

RIPK1 inhibits ZBP1-driven necroptosis during development.