Increased surface binding sites of insulin in ML236B (compactin)-resistant mutants of Chinese hamster cell line

Yasufumi Sato, Akinori Masuda, Mayumi Ono, Michihiko Kuwano

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)13-21
Number of pages9
JournalBiochemical and biophysical research communications
Volume117
Issue number1
DOIs
Publication statusPublished - 1983 Nov 30

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Increased surface binding sites of insulin in ML236B (compactin)-resistant mutants of Chinese hamster cell line'. Together they form a unique fingerprint.

  • Cite this