EFFECTS OF HERBIMYCIN-A AND VARIOUS SH-REAGENTS ON P60V-SRC KINASE-ACTIVITY INVITRO
EFFECTS OF HERBIMYCIN-A AND VARIOUS SH-REAGENTS ON P60V-SRC KINASE-ACTIVITY INVITRO
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DOI：
10.1016/s0006-291x(05)81053-8
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发表时间：
1990-11-30
影响因子：
3.1
通讯作者：
UEHARA, Y
中科院分区：
文献类型：
--
作者：
FUKAZAWA, H;MIZUNO, S;UEHARA, Y
除草剂A是一种逆转src家族癌基因引起的转化的抗生素。它在体外可能通过与p60v-src的反应性Sh基团(S)结合而使p60v-src失活。我们考察了不同SH试剂对p60V-src的影响，发现N-[对-(2-苯并咪唑基)苯基]马来酰亚胺(BIPM)或N-(9-acridinyl)马来酰亚胺(NAM)是该酶的有效钝化剂，而N-乙基马来酰亚胺(NEM)需要较高的浓度，而碘乙酰胺完全不能降低该酶的活性。然而，用NEM和碘乙酰胺预处理p60V-src免疫复合体，可以保护该酶不被去甲氧基霉素A、BIPM和NAM灭活。结果表明，除草霉素A结合的Sh基团(S)对该酶活性不是必需的，但位于活性中心附近。
Herbimycin A is an antibiotic 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-benzimidazoyly) 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.