ELISA试剂盒的另一种途径

<div style="border-bottom: 0px; border-left: 0px; padding-bottom: 0px; widows: 1; text-transform: none; list-style-type: none; text-indent: 0px; margin: 0px; padding-left: 0px; padding-right: 0px; font: 12px Helvetica, Arial, sans-serif; white-space: normal; letter-spacing: normal; color: rgb(0,0,0); border-top: 0px; border-right: 0px; word-spacing: 0px; padding-top: 0px; -webkit-text-stroke-width: 0px"> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;">端粒长度和结构的稳定与癌症发生密切相关，癌细胞通过端粒维持机制获得永生的能力。癌细胞的端粒维持，大多是通过端粒酶激活实现的。</span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><font face="宋体">不过，当端粒酶失活或不足的情况下，癌细胞还拥有另一种加长端粒的途径，即端粒替代延长机制（</font>ALT<font face="宋体">）找到了能在癌细胞中触发</font><font face="Calibri">ALT</font><font face="宋体">的有效工具，可以帮助人们深入理解</font><font face="Calibri">ALT</font><font face="宋体">的具体机制，端粒是由重复性</font><font face="Calibri">DNA</font><font face="宋体">组成的染色体末端保护结构，正常细胞每分裂一次，其端粒就会随之缩短，最终当端粒缩短到一定程度时，人</font><font face="Calibri">ELISA</font><font face="宋体">试剂盒细胞就会停止分裂或进行自毁。</font></span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;">绝大多数癌细胞可以通过上调端粒酶（负责加长端粒的酶），实现无限的细胞分裂。</span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><font face="宋体">大约有</font>5-15%<font face="宋体">的癌细胞会通过</font><font face="Calibri">ALT</font><font face="宋体">通路逃避细胞凋亡</font><font face="Calibri">ALT</font><font face="宋体">的一个重要标志是，在称为</font><font face="Calibri">PML</font><font face="宋体">小体（早幼粒细胞白血病小体）的特殊细胞核区域出现</font><font face="Calibri">RPA2</font><font face="宋体">蛋白（</font><font face="Calibri">replication protein A2</font><font face="宋体">）的累积。这种</font><font face="Calibri">PML</font><font face="宋体">小体中的关键组分是肿瘤抑制蛋白</font><font face="Calibri">PML</font><font face="宋体">。迄今为止，在多个人类细胞系中敲减了</font><font face="Calibri">ASF1</font><font face="宋体">。</font></span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><font face="宋体">这些细胞在三天内表现出了</font>ALT<font face="宋体">发生的迹象，这些细胞的染色质发生了结构改变，</font><font face="Calibri">RPA2</font><font face="宋体">也出现在</font><font face="Calibri">PML</font><font face="宋体">小体。显示</font><font face="Calibri">ASF1</font><font face="宋体">缺乏会增强端粒的重组，提高端粒长度的多样性，减少端粒酶催化亚基的表达。其中，端粒重组是</font><font face="Calibri">ALT</font><font face="宋体">的主要端粒维持机制。</font></span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><font face="宋体">尽管敲减</font>ASF1<font face="宋体">非常有用，不过这种情况可能并不会天然发生，因为</font><font face="Calibri">ASF1a</font><font face="宋体">和</font><font face="Calibri">ASF1b</font><font face="宋体">都是细胞生存和增殖所必需的蛋白。不过这些蛋白参与了端粒处的染色质塑造意味着，可以通过干扰染色质的结构来启动</font><font face="Calibri">ALT</font><font face="宋体">。人</font><font face="Calibri">ELISA</font><font face="宋体">试剂盒虽然一直推测染色质结构会对</font><font face="Calibri">ALT</font><font face="宋体">产生影响，但还未通过实验证明这一点。下一步将在更多的细胞系甚至动物体内敲减</font><font face="Calibri">ASF1</font><font face="宋体">，以便进一步解析</font><font face="Calibri">ALT</font><font face="宋体">通路的调控机制</font></span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> <p class="MsoNormal"><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><font face="宋体">。如果我们要在癌症治疗中成功靶标端粒长度或端粒酶，就需要深入理解</font>ALT<font face="宋体">，并对这一通路加以抑制这项研究提供了很实用的现在可以进一步理解</font><font face="Calibri">ALT</font><font face="宋体">通路，并在此基础上开发相应的抑制子。</font></span><span style="mso-spacerun:'yes';font-family:宋体;mso-ascii-font-family:Calibri;mso-hansi-font-family:Calibri;mso-bidi-font-family:'Times New Roman';font-size:9.0000pt;mso-font-kerning:1.0000pt;"><o:p></o:p></span></p> </div>