Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Stefan, C.
Right arrow Articles by Bollen, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stefan, C.
Right arrow Articles by Bollen, M.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 45, Issue 7 980-983, Copyright © 1996 by American Diabetes Association

ARTICLES

The inhibition of the insulin receptor by the receptor protein PC-1 is not specific and results from the hydrolysis of ATP

C Stefan, S Wera, W Stalmans and M Bollen
Division of Biochemistry, Faculty of Medicine, Catholic University of Leuven, Belgium.

The membrane protein plasma cell differentiation antigen 1 (PC-1) has been purified as an inhibitor of insulin receptor tyrosine kinase activity and has been implicated in the pathogenesis of NIDDM. However, we show here that PC-1 is a general protein kinase inhibitor in vitro and that this inhibition results from the hydrolysis of ATP by the intrinsic nucleotide pyrophosphatase activity of PC-1. Thus, the inhibition diminished with increasing ATP concentrations, and it was nullified when the ATP concentration was kept constant with a regenerating system or when ATP was added repetitively. When care was taken to avoid ATP depletion, PC-1 did not affect the insulin sensitivity of insulin receptor autophosphorylation. We conclude that the reported inhibition of insulin signaling by PC-1 does not result from a direct inhibition of the insulin receptor kinase activity.
Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 DiabetesHome page
K. Enjyoji, K. Kotani, C. Thukral, B. Blumel, X. Sun, Y. Wu, M. Imai, D. Friedman, E. Csizmadia, W. Bleibel, et al.
Deletion of Cd39/Entpd1 Results in Hepatic Insulin Resistance
Diabetes, September 1, 2008; 57(9): 2311 - 2320.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
L. Frittitta, S. Camastra, R. Baratta, B. V. Costanzo, M. D'Adamo, S. Graci, D. Spampinato, B. A. Maddux, R. Vigneri, E. Ferrannini, et al.
A Soluble PC-1 Circulates in Human Plasma: Relationship with Insulin Resistance and Associated Abnormalities
J. Clin. Endocrinol. Metab., October 1, 1999; 84(10): 3620 - 3625.
[Abstract] [Full Text] [PDF]

Home page
 FASEB J.Home page
H. DEISSLER, S. BLASS-KAMPMANN, E. BRUYNEEL, M. MAREEL, and M. F. RAJEWSKY
Neural cell surface differentiation antigen gp130RB13-6 induces fibroblasts and glioma cells to express astroglial proteins and invasive properties
FASEB J, April 1, 1999; 13(6): 657 - 666.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1996 by the American Diabetes Association.