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.
|Number of pages||9|
|Journal||Biochemical and biophysical research communications|
|Publication status||Published - 1983 Nov 30|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology