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Insulin receptor gene expression is reduced in cells from a progeric patient.

Abstract：

:We have studied a 15-year-old girl (P1) suffering from the Hutchinson-Gilford syndrome (progeria) associated with a severe insulin resistance. Insulin binding activity to P1 erythrocytes was 85% reduced when compared to that measured in ten normal controls matched for sex and age. This finding was confirmed in Epstein-Barr virus (EBV)-transformed lymphoblasts and depends on a reduction in insulin receptor number. Also the amount of total insulin receptors, [35S]methionine labeled and immunoprecipitated, was 90% reduced in P1 lymphoblasts when compared to controls. Next, we measured insulin receptor mRNA levels and we found undetectable levels of insulin receptor transcript in P1 EBV-transformed lymphoblasts, in the absence of any rearrangement of insulin receptor gene as evaluated by Southern blot analysis. The marked reduction in insulin receptor gene expression probably accounts for the severe insulin resistance presented by the patient. Despite extensive studies, the molecular basis of progeria is still unknown. The near complete absence of a molecule crucial in the transduction of cell growth and differentiation signals could be involved in the accelerated aging of the patient.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Briata P,Bellini C,Vignolo M,Gherzi R

doi

10.1016/0303-7207(91)90239-o

keywords:

subject

Has Abstract

pub_date

1991-01-01 00:00:00

pages

9-14

issue

1

eissn

0303-7207

issn

1872-8057

journal_volume

75

pub_type

杂志文章

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