Schumaker, Verne N.


Division
Biochemistry
Title
Faculty
Professor Emeritus

Contact Information

Email
Office
Boyer Hall 436
(310) 825-3531

Research Interest

Atherosclerosis, or hardening of the arteries, is responsible for heart attacks and strokes. A principle cause of atherosclerosis is an abundance of lipid in the diet, resulting in high levels of the serum lipoproteins. Therefore, it is important to study lipoprotein metabolism to learn how these particles are synthesized and secreted by living cells, and how this process is regulated. We are studying the molecular details of the biosynthesis of lipoproteins in hepatocyte cell culture, and have recently shown how the lipid and protein are assembled in the endoplasmic reticulum to form the lipoprotein particle.

Our next step will be to study the regulation of this process by hormonal factors which are known to play a role in atherosclerosis. Antibody usually does not kill the bacteria to which it binds; killing is left to other systems such as the serum complement system. The first component of complement, Cl, recognizes that antibody had bound to a pathogen, binds to the clustered antibody, and autoactivates. The activated Cl then initiates the classical complement pathway, leading to the elimination of the pathogen. Cl is a multisubunit complex formed of several smaller proteins, Clq, Clr and Cls. We are expressing Clr and Cls in a eucaryotic tissue culture system for site-directed mutagenesis and x-ray structural analysis. Our goal is to construct a functional model for the first component of complement. We hope that understanding the mechanism of activation of complement at the molecular level will allow enhancement of its pathogen killing function, and control of its deleterious effects in autoimmune disease.

Honors & Awards

  • Distinguished Teaching Award 
  • Herbert Newby McCoy Award 
  • John Simon Guggenheim Fellow 
  • NIH Fellow