Vaccinia virus-infected cells release a novel polypeptide functionally related to transforming and epidermal growth factors.
Vaccinia virus-infected cells release a novel polypeptide functionally related to transforming and epidermal growth factors.
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痘苗病毒感染的细胞释放出一种与转化因子和表皮生长因子功能相关的新型多肽。
DOI：
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发表时间：
1985
影响因子：
11.1
通讯作者：
Bernard Mosst
中科院分区：
文献类型：
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作者：
D. Twardzik;Joseph P. Brown;J. Ranchalis;G. Todaro;Bernard Mosst
最近发现痘苗病毒（VV）基因编码与转化生长因子（TGF-α）和表皮生长因子（EGF）具有结构同源性的多肽，这促使我们寻找具有预测生物活性的病毒诱导蛋白。发现 VV 感染的细胞培养物的上清液含有酸稳定的 Mr 25,000 多肽，该多肽与 EGF 竞争结合 EGF 膜受体。这种 VV 诱导的生长因子 (VGF) 与 EGF 和 TGF-α 一样，具有促有丝分裂作用，并在 TGF-β 存在的情况下刺激贴壁依赖性细胞生长。然而，VGF 在针对小型和大型 TGF-α 特异性的放射免疫测定中不发生交叉反应，并且与 EGF 抗血清表现出最小的交叉反应性。 2 小时内即可在培养基中检测到 VGF，感染后 12 小时出现最大量。 VGF 的水平与使用的 VV 的复数成正比。抑制病毒 DNA 合成可增强 VGF 的产生，这与 VGF 是 VV 编码的早期基因产物的假设一致。从感染 VV 的细胞中释放出的一种新型生长因子的证明，可能对病毒与宿主相互作用的性质产生重要影响。
The recent discovery, that a vaccinia virus (VV) gene encodes a polypeptide with structural homology to transforming growth factor (TGF-alpha) and epidermal growth factor (EGF), led us to look for a virus-induced protein with the predicted biological activity. The supernatants of VV-infected cell cultures were found to contain an acid stable Mr 25,000 polypeptide that competes with EGF for binding to EGF membrane receptors. This VV-induced growth factor (VGF) like EGF and TGF-alpha is mitogenic and stimulates anchorage-independent cell growth in the presence of TGF-beta. However, VGF did not cross-react in a radioimmunoassay specific for small and large forms of TGF-alpha and exhibited minimal cross-reactivity with antisera to EGF. VGF was detectable in the culture medium within 2 hr, and maximal amounts were present 12 hr after infection. The level of VGF was proportional to the multiplicity of VV used. Inhibition of viral DNA synthesis enhanced VGF production, consistent with the hypothesis that VGF is an early gene product encoded by VV. The demonstration of a novel growth factor, released from cells infected with VV, may have important implications regarding the nature of virus-host interactions.