Binding and tyrosine kinase activities of the insulin receptor on Epstein-Barr virus transformed lymphocytes from patients with Werner's syndrome.
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.
Kakehi
T
T
Department of Medicine, Kyoto University School of Medicine, Japan.
Kuzuya
H
H
Yoshimasa
Y
Y
Yamada
K
K
Okamoto
M
M
Nishimura
H
H
Imura
H
H
D000328:Adult; D005260:Female; D004854:Herpesvirus 4, Human; D006801:Humans; D007333:Insulin Resistance; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases / Q000378:metabolism*; D011972:Receptor, Insulin / Q000378:metabolism / Q000502:physiology*; D014898:Werner Syndrome / Q000378:metabolism / Q000503:physiopathology*
D011505:Protein-Tyrosine Kinases; D011972:Receptor, Insulin