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在人肝癌细胞７７２１中研究了酪氨酸蛋白激酶（ＴＰＫ）和蛋白激酶Ｃ（ＰＫＣ）的激活剂［分别为表皮生长因子（ＥＧＦ）和佛波酯（ＰＭＡ）］和各种蛋白激酶抑制剂对Ｎ－乙酰氨基葡萄糖转移酶Ｖ（ＧｎＴ－Ｖ）活力的影响，以探讨ＴＰＫ和ＰＫＣ对ＧｎＴ－Ｖ的调节。结果发现，ＥＧＦ或ＰＭＡ处理细胞４８ｈ后，ＧｎＴ－Ｖ的活力明显增高；蛋白激酶的非特异性抑制剂槲皮素和染料木黄酮（ｇｅｎｉｓｔｅｉｎ）在抑制ＴＰＫ和ＰＫＣ的同时，抑制ＧｎＴ－Ｖ的基础活力，并完全阻断ＥＧＦ或ＰＭＡ对ＧｎＴ－Ｖ的增高作用；ＴＰＫ的特异性抑制剂Ｔｙｒｐｈｏｓｔｉｎ－２５和ＰＫＣ的特异性抑制剂Ｄ－鞘氨醇分别应用时，各自只能部分地取消ＥＧＦ或ＰＭＡ对ＧｎＴ－Ｖ的诱导。但当Ｔｙｒｐｈｏｓｔｉｎ－２５和Ｄ－鞘氨醇同时加入培养基中则可完全阻断ＥＧＦ或ＰＭＡ对ＧｎＴ－Ｖ的诱导激活。蛋白质合成抑制剂环己亚胺和蛋白激酶抑制剂作用相仿，不但可抑制ＧｎＴ－Ｖ的基础活力，也可完全消除ＥＧＦ或ＰＭＡ对ＧｎＴ－Ｖ的激活。以上结果提示ＥＧＦ或ＰＭＡ通过蛋白激酶调节ＧｎＴ－Ｖ的酶蛋白合成，并且ＧｎＴ－Ｖ受到膜性ＴＰＫ和ＰＫＣ的双重调节，其中ｍ－ＴＰＫ较ｍ－ＰＫＣ更为重要。
Activators of tyrosine protein kinase (TPK) and protein kinase C (PKC) [epidermal growth factor (EGF) and phorbol ester (PMA), respectively] and various protein kinase inhibitors On the activity of N-acetylglucosaminyltransferase V (GnT-V), in order to investigate the regulation of GnT-V by TPK and PKC. The results showed that the activity of GnT-V was significantly increased after treated with EGF or PMA for 48 hours. The nonspecific inhibitors of protein kinase, quercetin and genistein, inhibited the base of GnT-V while inhibiting TPK and PKC And completely blocked the increase of GnT-V by EGF or PMA. When Tyrphostin-25, a specific inhibitor of TPK, and D-sphingosine, a specific inhibitor of PKC, were used, they could only partially eliminate EGF or Induction of GnT-V by PMA. However, when both Tyrphostin-25 and D-sphingosine were added to the medium, the induction of GnT-V activation by EGF or PMA was completely blocked. Protein synthesis inhibitors cycloheximide and protein kinase inhibitors similar role, not only can inhibit the basic activity of GnT-V, EGF or PMA can completely eliminate the activation of GnT-V. The above results suggest that EGF or PMA regulates GnT-V enzyme protein synthesis through protein kinase, and that GnT-V is double regulated by membrane TPK and PKC, of which m-TPK is more important than m-PKC.