南加州大学的一个研究小组利用X射线晶体学的方法跟踪大分子的运动，首次观察到了致癌蛋白LTag和关键的肿瘤抑制蛋白p53的结构。每一个"罪恶"的LTag（large T antigen的缩写）分子将六个p53捆绑起来，抑制它们的抑癌作用，该研究发表了9月1日的《Genes & Development》上。
有趣的是，p53蛋白通过阻止产生LTag病毒的复制来还击。胜负较强那一方决定。
“假如你有许多功能性p53蛋白分子，你就可以制服LTag蛋白，” USC分子与计算生物学教授，该研究的领导者Xiaojiang Chen说。
“p53蛋白是一种非常重要的肿瘤抑制蛋白，在许多癌症中均发生了突变。”匹兹堡大学生物科学系教授James Pipas说。
Pipas多年来从事LTag蛋白的研究，并且为它各种各样的生物学功能感到惊奇，包括高效的促癌作用等，在他的一个演讲中曾将LTag蛋白成为“宇宙中最令人惊奇的分子”。
Pipas称Chen的新研究为“一项非常重要的工作”，展示了一个健康细胞的防御肿瘤的防线是怎样瓦解的。
Pipas补充说，该研究可能导致设计抗癌药物的新技术的产生。
Chen的研究小组通过将一个LTag和六个p53分子的复合体结晶，成功的描述了LTag 与 p53分子之间的相互作用，它们之间一共存在着50,000个原子。
Chen称研究让他重新看待LTag和LTag的“亲代”——猿猴病毒 40（SV40）。SV40长期以来用作在培养细胞中诱导癌症的研究工具。
“不知道何故，SV40知道p53分子的重要性，从而命令致癌蛋白LTag通过身体相互接触作用靶向p53，改变p53的构象。” Chen说。
假如SV40成功做到这一点，结果就是新肿瘤产生了。
英文原文：
Cell's fight against cancer revealed Cell's fight against cancer revealed
By the painstaking use of X-ray crystallography to track motion in very large molecules, a University of Southern California-led research group has taken a first look at the life-or-death struggle of a cancer-causing protein – LTag – and a key tumor suppressor – p53.
Each villainous LTag (short for large T antigen) single-handedly ties up a tag-team of six p53 molecules, inhibiting their tumor-suppressant role, the researchers report in the Sept. 1 issue of Genes & Development.
Undeterred, the p53 fight back by preventing replication of the virus that produces LTag, known as an oncoprotein for its function in cancer growth.
The champion depends on which side is stronger and healthier.
"If you have a lot of functional p53, you can override large T antigen," said lead researcher Xiaojiang Chen, professor in molecular and computational biology in the USC College of Letters, Arts and Sciences.
Sometimes called the "Guardian of the Genome," a damaged p53 can leave a cell almost defenseless.
"p53 is a very important tumor suppressor that's mutated in a vast majority of all cancers," said James Pipas, professor of biological sciences at the University of Pittsburgh.
It was Pipas who, after studying LTag for many years and marveling at its varied biological functions – including highly efficient tumor promotion – named it "The Most Amazing Molecule in the Universe" in one of his presentations.
Pipas called Chen's new study "a very important piece of work" that shows how a healthy cell's tumor defenses break down.
"Understanding exactly how this works is going to be a critical step toward our understanding of tumor genesis," he said.
This, in turn, may lead to new techniques for designing tumor-fighting drugs, Pipas added.
Chen's team was able to describe the interplay between LTag and p53 by crystallizing the complex of one LTag and six p53 molecules, totaling more than 50,000 atoms between them.
"It's quite a technical achievement, because these are fairly large proteins," Pipas said.
Chen said his study gave him new respect for LTag and its parent, Simian Virus 40. SV40 has long been used as a research tool to induce cancers in cell cultures.
"Somehow this virus knows how important p53 is, and has this oncoprotein (LTag) to target it by physically interacting with it and changing its conformation," Chen said.
If the virus succeeds, the result is a new tumor.
