Matthew Summers

The Ohio State University United States of America

Matthew Summers received a Bachelor’s of Science degree in Biochemistry in 1997 from the University of Delaware. He then pursued his thesis work at the Wistar Institute and received a Ph.D. in Cell and Molecular Biology from the University of Pennsylvania in 2003. From 2004-2009 he performepostdoctoralal research at Stanford University and Genentech. In 2009, he joined the faculty at the Cleveland Clinic Lerner Research Institute as Assistant Staff. In 2015 he joined the Ohio State University and James Comprehensive Cancer Center as an Associate Professor. Research in the Summers lab focuses on the interplay between cellular checkpoints and the ubiquitin-proteasome system to regulate genome stability.

1books edited

1chapters authored

Latest work with IntechOpen by Matthew Summers

The human ubiquitin proteasome system (UPS) is comprised of nearly 1000 proteins. Although originally identified as a mechanism of protein destruction, the UPS has numerous additional functions and mediates central signaling events in myriad processes involved in both cellular and organismal health and homeostasis. Numerous pathways within the UPS are implicated in disease, ranging from cancer to neurodegenerative diseases such as Parkinson's. The goal of this book is to deliver a collection of synopses of current areas of UPS research that highlights the importance of understanding the biology of the UPS to identify disease-relevant pathways, and the need to elucidate the molecular machinations within the UPS to develop methods for therapeutic modulation of these pathways.

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Ubiquitin Proteasome System

Edited by Matthew Summers

Chapters authored

The Roles of Cullin RING Ligases and the Anaphase Promoting Complex/Cyclosome in the Regulation of DNA Double Strand Break Repair

By Debjani Pal and Matthew K. Summers

Historically, genome maintenance has been viewed as the largely independent activities of (1) ubiquitin ligases driving unidirectional cell cycle progression and, (2) the activity of cellular checkpoints that monitor DNA integrity and DNA replication. It is well established that the DNA damage response (DDR) checkpoint machinery promotes the activation of repair mechanisms in addition to opening a window for repair. Emerging evidence demonstrates an integrated network of the central cell cycle driving E3 ubiquitin ligases and the checkpoint machinery, as well as deubiquitinating enzymes, which intermittently cooperate and antagonize one another to define windows of checkpoint and repair activities to optimize genome stability and cellular health. A growing number of components of the ubiquitin machinery are involved in the DDR. Herein, we focus on the regulation of cell cycle checkpoints and the DNA repair mechanisms for double strand breaks (DSBs) by the coordinated activities of Cullin RING ligases (CRLs) and the anaphase promoting complex/cyclosome (APC/C).

Part of the book: Ubiquitination Governing DNA Repair

Matthew Summers

Latest work with IntechOpen by Matthew Summers

Ubiquitin Proteasome System

Chapters authored

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Debjani Pal