| Autor: |
Thompson, E. B., Smith, J. R., Bourgeois, S., Harmon, J. M. |
| Zdroj: |
Journal of Molecular Medicine; August 1985, Vol. 63 Issue: 15 p689-698, 10p |
| Abstrakt: |
Summary The evidence to date is compelling that steroid initiated cell lysis involves participation of the glucocorticoid receptor. Not only do the concentrations and specificity of hormones for cell lysis and receptor occupancy correspond, but also steroid resistant cells selected with or without prior mutagenesis often have altered receptors. The glucocorticoid receptor protein from humans and other species is a ~ 95,000 d, thiol group-containing monomer, prone to aggregation when “unactivated.” After having bound steroid and been “activated,” the monomeric steroid-receptor complex is altered in charge and shape so that its binding to chromatin and DNA is greatly enhanced. Simple measurement of numbers of receptor sites in cells from patients with various blood dyscrasias has given, in some diseases, good correlations between high numbers of receptor sites and good therapeutic response. These correlations are strongest for childhood acute lymphoblastic leukemia (ALL) and for non Hodgkins' lymphoma. In other diseases, notably acute myelogenous leukemia, such correlations have not been found. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
Full text from SpringerLink