Literature DB >> 381768

[Cell receptor defects as the cause of endocrine and metabolic diseases (author's transl)].

W Gerok.   

Abstract

The following pathogenetic mechanisms, exemplified by three diseases (diabetes mellitus, hyperthyroidism and familial hypercholesterolemia), are discussed: 1. The impaired interaction between a chemical signal and a specific receptor can be the cause of a disease. 2. The cause for an imparied interaction can be a defect of the receptor, i.e., a reduced number of receptors or an altered receptor affinity, or a wrong signal. 3. A defect of the receptor can be induced by exogenous influences or it can be determined genetically. 4. The receptor and the signal can be modified by their interaction: the number of receptors is reduced by high concentrations of the chemical signal or by increased degradation due to binding to the receptor. 5. The receptor concept opens new perspectives for the pathogenetic understanding, diagnosis and therapy of some diseases.

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Year:  1979        PMID: 381768     DOI: 10.1007/bf01477628

Source DB:  PubMed          Journal:  Klin Wochenschr        ISSN: 0023-2173


  49 in total

1.  Hormonal regulation of membrane receptors and cell responsiveness: a review.

Authors:  G P Tell; F Haour; J M Saez
Journal:  Metabolism       Date:  1978-10       Impact factor: 8.694

2.  Characteristics of a solubilized thyrotropin receptor from bovine thyroid plasma membranes.

Authors:  R L Tate; J M Holmes; L D Kohn; R J Winand
Journal:  J Biol Chem       Date:  1975-08-25       Impact factor: 5.157

3.  Lipoprotein receptors and genetic control of cholesterol metabolism in cultured human cells.

Authors:  M S Brown; J L Goldstein
Journal:  Naturwissenschaften       Date:  1975-08

4.  Determination of thyroid stimulating immunoglobulins (TSI) during the course of Graves' disease. A reliable indicator for remission and persistence of this disease?

Authors:  H Schleusener; R Finke; P Kotulla; K W Wenzel; H Meinhold; H D Roedler
Journal:  J Endocrinol Invest       Date:  1978-04       Impact factor: 4.256

5.  Insulin-receptor interaction in the obese-hyperglycemic mouse. A model of insulin resistance.

Authors:  C R Kahn; D M Neville; J Roth
Journal:  J Biol Chem       Date:  1973-01-10       Impact factor: 5.157

6.  Familial hypercholesterolemia in a large indred. Evidence for a monogenic mechanism.

Authors:  H G Schrott; J L Goldstein; W R Hazzard; M M McGoodwin; A G Motulsky
Journal:  Ann Intern Med       Date:  1972-05       Impact factor: 25.391

7.  Insulin-induced dissociation of its receptor into subunits: possible molecular concomitant of negative cooperativity.

Authors:  B H Ginsberg; C R Kahn; J Roth; P De Meyts
Journal:  Biochem Biophys Res Commun       Date:  1976-12-20       Impact factor: 3.575

8.  Regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in cultured human fibroblasts. Comparison of cells from a normal subject and from a patient with homozygous familial hypercholesterolemia.

Authors:  M S Brown; S E Dana; J L Goldstein
Journal:  J Biol Chem       Date:  1974-02-10       Impact factor: 5.157

9.  Insulin-dependent regulation of insulin receptor concentrations: a direct demonstration in cell culture.

Authors:  J R Gavin; J Roth; D M Neville; P de Meyts; D N Buell
Journal:  Proc Natl Acad Sci U S A       Date:  1974-01       Impact factor: 11.205

10.  Evidence for the identity of the major apoprotein in low density and very low density lipoproteins in normal subjects and patients with familial hyperlipoproteinemia.

Authors:  A M Gotto; W V Brown; R I Levy; M E Birnbaumer; D S Fredrickson
Journal:  J Clin Invest       Date:  1972-06       Impact factor: 14.808

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