Binding and tyrosine kinase activities of the insulin receptor on Epstein-Barr virus transformed lymphocytes from patients with Werner's syndrome.

Abstract

To assess the abnormalities of insulin receptor in patients with Werner's syndrome, we established Epstein-Barr virus transformed lymphocytes and studied the binding as well as kinase activities of insulin receptor. The insulin binding to both intact cells and WGA-purified insulin receptor preparations was within normal range. Autophosphorylation of the beta-subunit was not altered in patients with Werner's syndrome, and the receptors of these patients phosphorylated an exogenous substrate to a degree comparable to that of the normal participants. Taken together, these findings indicate that insulin resistance in Werner's syndrome likely is caused by a defect that cannot be detected by means used in the present study.

• Authors: T Kakehi, H Kuzuya, Y Yoshimasa, K Yamada, M Okamoto, H Nishimura, H Imura
• Journal: Journal of gerontology (J Gerontol) Vol. 43 Issue 2 Pg. M40-5 (Mar 1988) ISSN: 0022-1422 [Print] United States
• PMID: 2831266 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Protein-Tyrosine Kinases
• Receptor, Insulin

Topics

• Adult
• Female
• Herpesvirus 4, Human
• Humans
• Insulin Resistance
• Lymphocyte Activation
• Male
• Middle Aged
• Phosphorylation
• Protein-Tyrosine Kinases (metabolism)
• Receptor, Insulin (metabolism, physiology)
• Werner Syndrome (metabolism, physiopathology)