Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Colchicine and other antitubulin agents markedly enhanced the stimulation of DNA synthesis by combinations of various growth factors such as epidermal growth factor, insulin, fibroblast-derived growth factor, and vasopressin in serum-free cultures of several quiescent 3T3 mouse fibroblast cell lines. Enhancing effects were observed based on continuous incorporation of [3H]thymidine into DNA as well as by autoradiographic labeling of cell nuclei. The concentration of colchicine and podophyllotoxin required to produce half-maximal enhancement of DNA synthesis stimulated by epidermal growth factor and insulin was 25-50 nM. Lumicolchicine did not produce enhancing effects. The disassembly of microtubules resulting from the action of colchicine, Colcemid, and vinblastine did not inhibit the stimulation of DNA synthesis in quiescent Swiss 3T3 fibroblasts by fetal bovine serum. We conclude that the cytoplasmic microtubule network in 3T3 mouse fibroblasts does not exert a positive regulatory function in the initiation of DNA synthesis but rather can produce a constraint on the initial action of the peptide growth factors in serum-free media.
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PMID:Antitubulin agents enhance the stimulation of DNA synthesis by polypeptide growth factors in 3T3 mouse fibroblasts. 31 67

To evaluate the possible role of microtubules in the cellular action of vasopressin on the mammalian kidney, the effects of microtubule-disrupting agents were studied in vivo and in vitro. In vivo studies were done in rats in mild to moderate water diuresis induced by drinking 5% glucose. Microtubule-disrupting alkaloids, colchicine (0.1 mg/day) or vinblastine (0.08 mg/day), given intraperitoneally, did not change water and solute excretion itself, but blocked or markedly inhibited the antidiuretic response (increase in urine osmolality and decrease in urine flow) to exogenous vasopressin. Total solute excretion was unaffected by these two alkaloids and there were no substantial changes in excretion of sodium, potassium, or creatinine. Lumicolchicine, a derivative of colchicine that does not interact with microtubules, did not alter the antidiuretic response to exogenous vasopressin. Activities of adenylate cyclase in the renal medullary plasma membrane, and cyclic AMP phosphodiesterase and protein kinase in renal medullary cytosol, were not influenced by 10(-5)-10(-4) M colchicine or vinblastine in vitro. Studies on the subcellular distribution of microtubular protein (assessed as [(3)H]colchicine-binding protein) in renal medulla shows that this protein is contained predominantly in the cytosol. Particulate fractions, including plasma membrane, contain only a minute amount (less than 6%) of the colchicine-binding activity. The results suggest that the integrity of cytoplasmic microtubules in cells of the distal nephron is required for the antidiuretic action of vasopressin, probably in the sites distal to cyclic AMP generation in the mammalian kidney.
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PMID:Effects of colchicine and vinblastine on the cellular action of vasopressin in mammalian kidney. A possible role of microtubules. 436 87