CELL SIGNALING, KINASE, AND CHEMOTHERAPY 

New concepts from bench to bedside

Kinase-mediated signaling plays essential roles in cell growth, differentiation and homeostasis. Kinases signal by switching between “on” and “off” conformational states, and many inputs regulate the activity of each specific kinase. Abnormal kinase activity, often the result of mutation, is associated with many cancers, and kinase inhibitors have become a highly successful and growing class of anti-cancer agents. This 2016 American Society for Biochemistry and Molecular Biology annual meeting symposium will focus on emerging insights into the molecular mechanisms by which kinase activity is regulated and how these insights are influencing strategies to target kinase activity in cancer.

Molecular mechanism

Intra- and intermolecular interactions, phosphorylation and combinations of such events have been shown to influence kinase activity. The first session will highlight new insights into the molecular mechanisms governing the activity of key kinases, how the activity of these kinases becomes deregulated in disease and how an understanding of mechanism has influenced strategies to target kinases therapeutically.

Spatiotemporal control

Movement of kinases both within membranes and to and from different membrane compartments is known to affect the nature and timing of kinase signaling. The second session will highlight state-of-the-art studies of the movement of specific kinases during signaling and how location modulates signaling activity.

Therapeutic strategies

New strategies for designing kinase inhibitors are discussed in terms of pseudokinases, active kinases and allosteric sites. In the third session, new approaches for discovering target genes will be described as will new targets that lie downstream of kinases.

New roles for old kinases

Kinases are dynamic molecular switches that easily can be hijacked to create oncogenes that drive cancers. The final session will discuss how both kinases and pseudokinases can drive tumors and introduce new roles for PKC and PKA as tissue-specific tumor drivers and tumor suppressors.

Organizers

Dan Leahy

Dan Leahy, Johns Hopkins University School of Medicine

Susan Taylor

Susan Taylor, University of California, San Diego