Cytochalasin B: Inhibition of Glucose and Glucosamine Transport

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Mechanism of inhibition of human glucose transporter GLUT1 is conserved between cytochalasin B and phenylalanine amides.

Cancerous cells have an acutely increased demand for energy, leading to increased levels of human glucose transporter 1 (hGLUT1). This up-regulation suggests hGLUT1 as a target for therapeutic inhibitors addressing a multitude of cancer types. Here, we present three inhibitor-bound, inward-open structures of WT-hGLUT1 crystallized with three different inhibitors: cytochalasin B, a nine-membered...

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Inhibition of unidirectional influx of glucose into the isolated perfused dog brain by cytochalasin B.

Cytochalasin B, a fungal metabolite, has been shown to inhibit hexose transport in a variety of cellular types, including erythrocytes (Bloch, 1973), leucocytes (Zigmond & Hirsch, 1972), adipose-cell ‘ghosts’ (Czech et al., 1973), fibroblasts and liver cells (Kletzien et al., 1972) and HeLa cells (Mitzel & Wilson, 1972). Studies of effects of cytochalasin B on hexose transport in the nervous sy...

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Cytochalasin B

Cytochalasin B competitively inhibits the transport of uridine and thymidine by Novikoff rat hepatoma cells growing in suspension culture with apparent K(i)'s of 2 and 6 microM, respectively, but has no effect on the intracellular phosphorylation of the nucleosides. Choline transport is not affected by cytochalasin B. Results from pulse-chase experiments indicate that cytochalasin B has no dire...

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Cytochalasin B

Cytochalasin B, a mold metabolite, has been shown to inhibit cytokinesis and motility (3), morphogenie development (18), endocytosis (5), and the transport of sugars (8-10, 12). I t has also been demonstrated that this drug inhibits the stimuatcd elaboration of extracellular substances from glands-the release of thyroxine from the thyroid gland after stimulation by thyroid-stimulating hormone (...

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Inhibition of DNA synthesis in adrenocortical cells by cytochalasin B

ACTH inhibits DNA synthesis in normal rat and mouse tumor Y-1 adrenocortical cells within the same concentration range that it stimulates steroidogenesis. These processes can be independently regulated as demonstrated by the divergent actions of cytochalasin B on these cells. In the normal cells, cytochalasin B does not increase steroidogenesis in serum-free or serum-containing media, and it de...

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ژورنال

عنوان ژورنال: Proceedings of the National Academy of Sciences

سال: 1972

ISSN: 0027-8424,1091-6490

DOI: 10.1073/pnas.69.6.1430