FACTOR-XIIIA-CATALYZED CROSS-LINKING OF PLATELET AND MUSCLE ACTIN - REGULATION BY NUCLEOTIDES
FACTOR-XIIIA-CATALYZED CROSS-LINKING OF PLATELET AND MUSCLE ACTIN - REGULATION BY NUCLEOTIDES
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DOI：
10.1016/0304-4165(80)90386-4
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发表时间：
1980-01-01
期刊：
影响因子：
--
通讯作者：
VEIS, A
中科院分区：
文献类型：
--
作者：
COHEN, I;BLANKENBERG, TA;VEIS, A
来自人血小板或兔骨骼肌的肌动蛋白可以作为因子XIIIa的底物。后者催化1.5-2 mol单丹酰尸胺/mol兔肌动蛋白和0.5mol/mol血小板肌动蛋白的掺入。高度交联的血小板和肌肉肌动蛋白聚合物的形式在没有添加胺，表明受体和供体网站的存在。如所预期的，交联是γ。谷氨酰-ε-赖氨酸键，平均为0.3-0.4 mol二肽/mol血小板肌动蛋白。ATP、ADP、GTP和CTP可阻止交联和胺掺入，但AMP和环AMP则不能。这些核苷酸可能在肌肉和非肌肉系统中具有重要的调节作用。
Actin from human blood platelets or rabbit skeletal muscle can serve as substrate for factor XIIIa. The latter catalyzes the incorporation of 1.5-2 mol monodansylcadaverine/mol rabbit actin and 0.5 mol/mol platelet actin. Highly cross-linked platelet and muscle actin polymers form in the absence of added amines, indicating the presence of acceptor and donor sites. As expected, the cross-link was a .gamma.-glutamyl-.epsilon.-lysine bond, with an average of 0.3-0.4 mol dipeptide/mol platelet actin. Cross-linking and amine incorporation are prevented by ATP, ADP, GTP and CTP, but not by AMP and cyclic AMP. These nucleotides may have an important regulatory role in muscle and non-muscle systems.