Increased surface binding sites of insulin in ML236B (compactin)-resistant mutants of Chinese hamster cell line.
Mutants resistant to ML236B (compactin) were isolated from the Chinese hamster lung V79 cell line (1). Three ML236B-resistant mutants, MF-1, MF-2 and MF-3, were enhanced in insulin-specific binding activity about 2 to 3 times over the parental V79 cell lines. Compared to V79, endocytosis of insulin was also increased 2 to 3-fold in ML236B-resistant mutants than V79. Scatchard analysis showed that 5,000 insulin binding sites per cell in V79 and 16,000 in a NL236B-resistant clone, MF-2. Insulin receptors in mutant and parental strains are down-regulated to a similar extent in the parental V79 treated with an excess insulin. This is the first somatic cell mutant with increased surface binding sites for insulin.
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002460:Cell Line; D002999:Clone Cells; D006224:Cricetinae; D003412:Cricetulus; D004351:Drug Resistance; D007328:Insulin / Q000031:analogs & derivatives* / Q000378:metabolism; D007700:Kinetics; D008148:Lovastatin / Q000031:analogs & derivatives*; D008168:Lung; D009154:Mutation; D009281:Naphthalenes / Q000494:pharmacology*; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism*
D000900:Anti-Bacterial Agents; D007328:Insulin; D009281:Naphthalenes; C008147:insulin, iodo-; C012258:mevastatin; D008148:Lovastatin; D011972:Receptor, Insulin