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(jié)構(gòu)的穩(wěn)定與癌癥發(fā)生密切相關(guān)，癌細(xì)胞通過端粒維持機(jī)制獲得永生的能力。癌細(xì)胞的端粒維持，大多是通過端粒酶激活實(shí)現(xiàn)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(dāng)端粒酶失活或不足的情況下，癌細(xì)胞還擁有另一種加長端粒的途徑，即端粒替代延長機(jī)制（</font>ALT<font face="宋體">）找到了能在癌細(xì)胞中觸發(fā)</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(jī)制，端粒是由重復(fù)性</font><font face="Calibri">DNA</font><font face="宋體">組成的染色體末端保護(hù)結(jié)構(gòu)，正常細(xì)胞每分裂一次，其端粒就會隨之縮短，最終當(dāng)端粒縮短到一定程度時(shí)，人</font><font face="Calibri">ELISA</font><font face="宋體">試劑盒細(xì)胞就會停止分裂或進(jìn)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(shù)癌細(xì)胞可以通過上調(diào)端粒酶（負(fù)責(zé)加長端粒的酶），實(shí)現(xiàn)無限的細(xì)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(xì)胞會通過</font><font face="Calibri">ALT</font><font face="宋體">通路逃避細(xì)胞凋亡</font><font face="Calibri">ALT</font><font face="宋體">的一個(gè)重要標(biāo)志是，在稱為</font><font face="Calibri">PML</font><font face="宋體">小體（早幼粒細(xì)胞白血病小體）的特殊細(xì)胞核區(qū)域出現(xiàn)</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(guān)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(gè)人類細(xì)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(xì)胞在三天內(nèi)表現(xiàn)出了</font>ALT<font face="宋體">發(fā)生的跡象，這些細(xì)胞的染色質(zhì)發(fā)生了結(jié)構(gòu)改變，</font><font face="Calibri">RPA2</font><font face="宋體">也出現(xiàn)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(qiáng)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(dá)。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(jī)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(fā)生，因?yàn)?lt;/font><font face="Calibri">ASF1a</font><font face="宋體">和</font><font face="Calibri">ASF1b</font><font face="宋體">都是細(xì)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(zhì)塑造意味著，可以通過干擾染色質(zhì)的結(jié)構(gòu)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(zhì)結(jié)構(gòu)會對</font><font face="Calibri">ALT</font><font face="宋體">產(chǎn)生影響，但還未通過實(shí)驗(yàn)證明這一點(diǎn)。下一步將在更多的細(xì)胞系甚至動物體內(nèi)敲減</font><font face="Calibri">ASF1</font><font face="宋體">，以便進(jìn)一步解析</font><font face="Calibri">ALT</font><font face="宋體">通路的調(diào)控機(jī)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(biāo)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(xiàng)研究提供了很實(shí)用的現(xiàn)在可以進(jìn)一步理解</font><font face="Calibri">ALT</font><font face="宋體">通路，并在此基礎(chǔ)上開發(fā)相應(yīng)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>