J. Lipid Res. Did you know there is a large type edition? Click here.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Peterson, A. S.
Right arrow Articles by Young, S. G.
PubMed
Right arrow Articles by Peterson, A. S.
Right arrow Articles by Young, S. G.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Journal of Lipid Research, Vol. 49, 1595-1599, July 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology


Commentary

Errata. PCSK9 function and physiology1

Andrew S. Peterson2,*, Loren G. Fong{dagger} and Stephen G. Young, Associate Editor2,{dagger},§

* Department of Molecular Biology, Genentech, South San Francisco, CA
{dagger} Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA
§ Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA

1 See referenced articles, J. Lipid Res. 2008, 49: 1303–1311 and 1333–1343.

Supported by NIH grants U01 HL66621 and R01 HL087228 (to SGY).

Conflict of interest disclosures: Dr. Andrew Peterson is an employee of Genentech, a pharmaceutical and biotechnology company. Dr. Stephen G. Young is an employee of UCLA but periodically consults for Genentech and Isis Pharmaceuticals.

2 To whom correspondence should be addressed. e-mail: sgyoung{at}mednet.ucla.edu (S.G.Y) or peterson.andrew{at}gene.com (A.S.P)


ABSTRACT

PCSK9 has exploded onto center stage of plasma cholesterol metabolism, raising hopes for a new strategy to treat hypercholesterolemia. PCSK9 in a plasma protein that triggers increased degradation of the LDL receptor. Gain-of-function mutations in PCSK9 reduce LDL receptor levels in the liver, resulting in high levels of LDL cholesterol in the plasma and increased susceptibility to coronary heart disease. Loss-of-function mutations lead to higher levels of the LDL receptor, lower LDL cholesterol levels, and protection from coronary heart disease. Two papers in this issue of the Journal of Lipid Research exemplify the rapid pace of progress in understanding PCSK9 molecular interactions and physiology. Dr. Shilpa Pandit and coworkers from Merck Research Laboratories describe the functional basis for the hypercholesterolemia associated with gain-of-function missense mutations in PCSK9. Dr. Jay Horton's group at UT Southwestern describe the kinetics and metabolism of PCSK9 and the impact of PCSK9 on LDL receptors in the liver and adrenal gland.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2008 by the American Society for Biochemistry and Molecular Biology.