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Biomedical subjects

J D Baxter

Publications and source records attributed to J D Baxter.

At least 271 records · Page 15Linked to original sources
PubMed1975

Chemodectomas of the head and neck.

Chemodectomas of the head and neck are reviewed. Their clinical picture, frequent multicentric origin, microscopie and macroscopic picture are discussed as well as their roentgenologic appearance. The role of angiography in their diagnosis is emphasized.

Adolescent↗
PubMed1973

Nuclear binding of steroid receptors: comparison in intact cells and cell-free systems.

In regulating gene expression in mammalian tissues, steroid hormones bind to cytoplasmic receptors and the resulting complex associates with the nucleus. In an attempt to study this nuclear association under more precisely controlled conditions, we examined the binding of receptor-[(3)H]steroid complexes to isolated nuclei. Two systems were used: the glucocorticoid-responsive hepatoma cell and the estrogen-sensitive immature rat uterus. Cell-free nuclear binding resembles that observed in the intact cell; it requires the receptor-steroid complex in the appropriate form ("active" complex); it is of high affinity; and it appears to involve about 4000 nuclear acceptor sites per haploid genome. Furthermore, whether binding occurs in intact cells or in cell-free extracts, complexes dissociate from nuclei at similar rates, and the ability of NaCl to extract either type of nuclear-bound complex and the sedimentation velocities of the extracted complexes are identical. Despite these similarities, acceptor sites detected in isolated nuclei differ from those of intact cells, since in neither hepatoma cells nor in the uterus do complexes bound to the nuclei of intact cells prevent further cell-free binding. We conclude that receptor-steroid complexes bind to acceptor sites in isolated nuclei that are chemically similar to, but topographically different from, those of the intact cell.

Animals↗
PubMed1972

Cellular site of glucocorticoid-receptor complex formation.

The cellular site of binding of dexamethasone by specific glucocorticoid receptors in cultured hepatoma cells was investigated with the use of certain mercurials. p-Chloromercuribenzene sulfonate and p-chloromercuribenzoate inhibit the binding of steroid by receptors in cell-free extracts, but they allow the steroid-receptor complex to form in whole cells. In contrast, HgCl(2) inhibits binding both in extracts and cells. Since both organic mercury compounds, unlike HgCl(2), do not readily enter intact cells, it appears that the specific steroid binding occurs inside the cell rather than at the cell membrane.

Animals↗
PubMed1972

Role of DNA and specific cytoplasmic receptors in glucocorticoid action.

Glucocorticoids induce tyrosine aminotransferase (EC 2.6.1.5) synthesis in cultured rat hepatoma cells. These steroids penetrate the cell membrane and bind to specific cytoplasmic receptor proteins. The resulting complex binds to the nucleus. This nuclear binding has now been studied in a cell-free preparation. The reaction appears to require a temperature-dependent modification of the steroid-receptor complex. There is a fixed number of nuclear sites that are half saturated at a complex concentration of 6 to 24 x 10(-11) M. Treatment with deoxyribonuclease destroys nuclear-binding capacity. The complex also binds to purified HTC cell DNA with characteristics similar to the binding to isolated nuclei, and, as in intact cells, receptors complexed with an anti-inducer steroid bind very poorly to DNA. These data suggest that the nuclear sites for binding steroid-receptor complexes are on the DNA. Since the extent of complex binding to purified DNA exceeds that observed with isolated nuclei, chromosomal proteins may act to restrict binding to certain regions of the DNA. These studies suggest that steroid hormones stimulate the synthesis of specific proteins by affecting the transcription of structural or regulatory genes.

Binding Sites↗
PubMed1971

Glucocorticoid receptors in lymphoma cells in culture: relationship to glucocorticoid killing activity.

Mouse lymphoma cells in culture which are killed by adrenal steroids contain specific cortisol receptors that may be involved in the initial events of hormone action. The similarity of these receptors to those in hepatoma tissue culture cells, where adrenal steroids induce tyrosine aminotransferase, suggests that certain aspects of steroid action are similar in the two systems. In three steroid-resistant lymphoma cell populations specific binding was less than in the parent lines, suggesting that conversion to steroid resistance may be associated with changes in specific steroid binding.

17-Ketosteroids↗