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trichosanthin/atrofia
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Trichosanthin induces atresia of ovarian follicles and inhibits steroidogenesis in gonadotropin-primed immature mice.
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1. Immature mice were induced to ovulate by injections of pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin spaced 48 hr apart. 2. Trichosanthin (TCS), a protein purified from tubers of Trichosanthes kirilowii (Family Cucurbitaceae), was administered respectively 24 hr before,
Receptor-mediated endocytosis of trichosanthin in choriocarcinoma cells.
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Trichosanthin (TCS) is a ribosome inactivating protein (RIP). It is generally believed that its many biological activities act through inhibition of ribosomes resulting in a decrease in protein synthesis. It has been hypothesized that the rate of entry of TCS into cells to reach ribosomes is an
Mechanism of the specific neuronal toxicity of a type I ribosome-inactivating protein, trichosanthin.
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The aim was to study the mechanism of neuronal toxicity, the cellular pathway, and the glial cell reactions induced by trichosanthin (TCS), a type I ribosome-inactivating protein (RIP). Ricin A chain (RTA) was included for comparison. TCS, RTA, and fluorescein isothiocyanate (FITC)-labeled TCS and
Transverse relaxation optimized 3D and 4D 15n/15N separated NOESY experiments of 15N labeled proteins.
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NMR studies of protein structures require knowledge of spectral assignments through correlation spectroscopy and the measurement of dipolar interactions by NOESY-type experiments. In order to obtain NOEs for protons with degenerate chemical shifts, which is particularly common for large proteins
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