ELISA試劑盒的另一種途徑

<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:宋體;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;">端粒長度和結構的穩定與癌癥發生密切相關，癌細胞通過端粒維持機制獲得永生的能力。癌細胞的端粒維持，大多是通過端粒酶激活實現的。</span><span style="mso-spacerun:'yes';font-family:宋體;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:宋體;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="宋體">不過，當端粒酶失活或不足的情況下，癌細胞還擁有另一種加長端粒的途徑，即端粒替代延長機制（</font>ALT<font face="宋體">）找到了能在癌細胞中觸發</font><font face="Calibri">ALT</font><font face="宋體">的有效工具，可以幫助人們深入理解</font><font face="Calibri">ALT</font><font face="宋體">的具體機制，端粒是由重復性</font><font face="Calibri">DNA</font><font face="宋體">組成的染色體末端保護結構，正常細胞每分裂一次，其端粒就會隨之縮短，最終當端粒縮短到一定程度時，人</font><font face="Calibri">ELISA</font><font face="宋體">試劑盒細胞就會停止分裂或進行自毀。</font></span><span style="mso-spacerun:'yes';font-family:宋體;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:宋體;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;">絕大多數癌細胞可以通過上調端粒酶（負責加長端粒的酶），實現無限的細胞分裂。</span><span style="mso-spacerun:'yes';font-family:宋體;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:宋體;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="宋體">大約有</font>5-15%<font face="宋體">的癌細胞會通過</font><font face="Calibri">ALT</font><font face="宋體">通路逃避細胞凋亡</font><font face="Calibri">ALT</font><font face="宋體">的一個重要標志是，在稱為</font><font face="Calibri">PML</font><font face="宋體">小體（早幼粒細胞白血病小體）的特殊細胞核區域出現</font><font face="Calibri">RPA2</font><font face="宋體">蛋白（</font><font face="Calibri">replication protein A2</font><font face="宋體">）的累積。這種</font><font face="Calibri">PML</font><font face="宋體">小體中的關鍵組分是腫瘤抑制蛋白</font><font face="Calibri">PML</font><font face="宋體">。迄今為止，在多個人類細胞系中敲減了</font><font face="Calibri">ASF1</font><font face="宋體">。</font></span><span style="mso-spacerun:'yes';font-family:宋體;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:宋體;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="宋體">這些細胞在三天內表現出了</font>ALT<font face="宋體">發生的跡象，這些細胞的染色質發生了結構改變，</font><font face="Calibri">RPA2</font><font face="宋體">也出現在</font><font face="Calibri">PML</font><font face="宋體">小體。顯示</font><font face="Calibri">ASF1</font><font face="宋體">缺乏會增強端粒的重組，提高端粒長度的多樣性，減少端粒酶催化亞基的表達。其中，端粒重組是</font><font face="Calibri">ALT</font><font face="宋體">的主要端粒維持機制。</font></span><span style="mso-spacerun:'yes';font-family:宋體;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:宋體;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="宋體">盡管敲減</font>ASF1<font face="宋體">非常有用，不過這種情況可能并不會天然發生，因為</font><font face="Calibri">ASF1a</font><font face="宋體">和</font><font face="Calibri">ASF1b</font><font face="宋體">都是細胞生存和增殖所必需的蛋白。不過這些蛋白參與了端粒處的染色質塑造意味著，可以通過干擾染色質的結構來啟動</font><font face="Calibri">ALT</font><font face="宋體">。人</font><font face="Calibri">ELISA</font><font face="宋體">試劑盒雖然一直推測染色質結構會對</font><font face="Calibri">ALT</font><font face="宋體">產生影響，但還未通過實驗證明這一點。下一步將在更多的細胞系甚至動物體內敲減</font><font face="Calibri">ASF1</font><font face="宋體">，以便進一步解析</font><font face="Calibri">ALT</font><font face="宋體">通路的調控機制</font></span><span style="mso-spacerun:'yes';font-family:宋體;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:宋體;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="宋體">。如果我們要在癌癥治療中成功靶標端粒長度或端粒酶，就需要深入理解</font>ALT<font face="宋體">，并對這一通路加以抑制這項研究提供了很實用的現在可以進一步理解</font><font face="Calibri">ALT</font><font face="宋體">通路，并在此基礎上開發相應的抑制子。</font></span><span style="mso-spacerun:'yes';font-family:宋體;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>