Alexandra C. Newton, Ph.D.

Professor of Pharmacology
University of California, San Diego

Dr. Newton studies the molecular mechanisms underlying how cells process information in health and in disease.   Cellular homeostasis depends on precise control of the balance between “go” and “stop” signals controlled by protein kinases and protein phosphatases, enzymes with opposing functions.  Deregulation of this balance leads to pathophysiological states, driving either pro-survival diseases such as cancer or degenerative diseases such as Alzheimer’s disease.  The Newton lab focuses, in particular, on the structure, function, and regulation of protein kinase C and how aberrant function contributes to the pathophysiologies of cancer and Alzheimer’s disease.  Understanding the molecular basis for how protein kinase C is deregulated in these diseases has potential for novel therapeutic strategies.  Dr. Alexandra Newton received her Ph.D. in Chemistry from Stanford University and her postdoctoral training in Daniel E. Koshland's laboratory at the University of California, Berkeley.   

Funded Research

Project Description Researchers Funding
Alzheimer Disease-Associated Mutations in Protein Kinase C

This proposal addresses whether a key protein that is turned off in cancer, a disease characterized by uncontrolled cellular growth and survival, is excessively active in Alzheimer’s disease, a degenerative disease. This protein, called protein kinase C, is an information processor, or “signal transducer,” that regulates cellular activities. Its activity needs to be precisely balanced to maintain normal cellular function. Reduced function promotes cell survival, a hallmark of cancer.

2016
$250,000
PKC Mutations and Alzheimer's Disease

The goal of this project is to analyze how Alzheimer’s disease (AD)-associated mutations in a key signaling molecule, protein kinase C α (PKCα), contribute to disease pathogenesis. PKCα plays a pivotal role in tuning the signaling output of cells and, as such, is frequently mutated in human cancers. The Alzheimer’s Genome Project™ led by Tanzi and colleagues has identified unique mutations in PKCα that co-segregate with AD in families with the disease.

2015
$220,000
Alzheimer’s disease-associated mutations in PKCα: analysis of aberrant signaling output
The goal of this project is to analyze how Alzheimers Disease (AD)-associated mutations in a key signaling molecule, protein kinase C α (PKCα), alter its function. PKCα plays a pivotal role in tuning the signaling output of cells and, as such, is frequently mutated in human cancers. The Alzheimer’s Genome Project led by Tanzi and colleagues has identified unique mutations in PKCα that co-segregate with AD in families with the disease.
2014
$100,000