| Literature DB >> 2175179 |
H Fukazawa1, S Mizuno, Y Uehara.
Abstract
Herbimycin A is an antiobiotic which reverses transformation caused by src family oncogenes. It inactivates p60v-src in vitro, possibly by binding to reactive SH-group(s) of the kinase. We examined effects of various SH-reagents on p60v-src and observed that N-[p-(2-benzimidazolyl)phenyl]maleimide (BIPM) or N-(9-acridinyl)maleimide (NAM) were potent inactivators of the kinase, whereas N-ethylmaleimide (NEM) required high concentrations, and iodoacetamide was totally ineffective in reducing the kinase activity. Pretreatment of p60v-src immune-complex with NEM and iodoacetamide, however, protected the kinase from inactivation by herbimycin A, BIPM, and NAM. The results suggest that SH-group(s) to which herbimycin A binds is not essential for the kinase activity, but is positioned in the vicinity of the active center.Entities:
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Year: 1990 PMID: 2175179 DOI: 10.1016/s0006-291x(05)81053-8
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575