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Biomedical subjects

U Gehring

Publications and source records attributed to U Gehring.

At least 91 records · Page 5Linked to original sources
PubMed1980

Specific receptors control steroid sensitivity in lymphoma cell hybrids.

Hybrids between different mouse lymphoma cell lines were prepared. 3 sub-lines of S49.1 were used: one of them was glucocorticoid-sensitive (wild-type, wt), the others were resistant with defects either in receptor binding (r-) or in nuclear transfer of the receptor-glucocorticoid complex (nt-). These cells were hybridized with another glucocorticoid-resistant lymphoma, EL4, which is of the nt- phenotype. wild-type glucocorticoid sensitivity was dominant over nt- resistance, and S49.1 wt X EL4 hybrids contained glucocorticoid receptors of both parental cell types. The r- and nt- phenotypes did not complement, suggesting that both defects occurred in the same polypeptide. S49.1 wt X EL4 hybrids produced resistant cells at 3 XC 10(-4) per cell per generation. Sensitive hybrid cell clones were treated with high glucocorticoid doses to select for resistant segregants. The majority of these segregants had lost one chromosome. The concomitant loss of the wild-type S49.1 receptor was observed upon transition from sensitivity to resistance. These results provide direct evidence for the hemizygosity of the glucocorticoid receptor gene in S49.1 cells. Thus, the cell system described here is suitable for assigning the glucocorticoid receptor gene to a specific mouse chromosome.

Animals↗
PubMed1980

[Molecular mechanisms of steroid hormone action (author's transl)].

The present survey is an attempt to present a unifying model for the mechanism of action of steroid hormones. Out of an overwhelming body of experimental observations with various cell and hormone systems a few representative examples are presented. The following sequence of events is outlined: a) penetration of the steroid hormone into target cells, b) binding to the active conformation of a specific cytoplasmic receptor, c) activation of the receptor-steroid complex, d) binding of the activated complex to chromatin, e) regulation of specific RNA and protein syntheses and by that means expression of target cell specific responses. Some effects of steroid hormones, however, cannot be explained by this model of steroid hormone action.

Aldosterone↗
PubMed1979

Somatic cell fusion in the study of glucocorticoid action.

The basic phenomena of cell fusion and hybrid cell formation are briefly described and the potential of somatic cell hybridization in studies on the expression of differentiated cellular functions is discussed. The technique of cell hybridization has been applied to two types of cellular responses to glucocorticoids. The induction of specific proteins has been investigated in hybrids of inducible cells with uninducible cells. Most studies dealt with the liver-specific enzyme tyrosine aminotransferase, whose inducibility was extinguished in the majority of the hybrids between hepatoma and nonliver cells. However, upon chromosome segregation, inducibility reappeared in some of these hybrid cells. The current ideas about cellular control of inducibility are discussed. The other major glucocorticoid-responsive system investigated in cell hybridization studies consists of lymphoid cells which are killed when exposed to the steroid. Such sensitive cells were hybridized with several types of glucocorticoid-resistant lymphoid lines, and sensitivity was found to be dominant over resistence. Hybrids between sensitive and resistant lymphoid cells, however, showed an increase in the frequency at which resistance occurred as compared to the rate observed with the wild-type parental cells. No complementation to steroid sensitivity was found in hybrids between different types of resistant cells with defects in the glucocorticoid-specific receptor system.

Animals↗
PubMed1976

Caffeine, cyclic AMP and postreplication repair of mammalian cell DNA.

The methylxanthines, caffeine and theophylline, inhibit postreplication repair of DNA in mammalian cells. Because they also inhibit cyclic AMP phosphodiesterase, it was thought that there might be some connection between concentrations of cyclic AMP and postreplication repair. We tested this possibility by performing DNA sedimentation experiments with a cyclic AMP-resistant mouse lymphoma cell mutant and its wild-type counterpart. The results show that there is no connection between cellular cyclic AMP concentrations and the rate of postreplication repair. Therefore, it is more likely that caffeine and theophylline inhibit postreplication repair by some other means, such as by binding to DNA.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1972

Glucocorticoid action on hybrid clones derived from cultured myeloma and lymphoma cell lines.

Cells of a cloned myeloma line from a Balb/c mouse contain specific cytoplasmic glucocorticoid receptors and are killed by dexamethasone. Cells of a lymphoma line (from mouse strain C57BL) also contain specific glucocorticoid receptors but are resistant to the steroid. Cells of two hybrid clones with widely differing chromosome numbers, derived by fusion between the resistant lymphoma and the sensitive myeloma, contain specific glucocorticoid receptors with similar binding properties as the parental receptors and are killed by dexamethasone. Since the lethal effect of the steroid is expressed in the hybrid cells, failure of the parent lymphoma line to be affected by dexamethasone is probably not due to an inhibitor of the lethal reaction.

Androstenes↗