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ERCC1 人切除修復(fù)交叉互補(bǔ)基因1
廣州健侖生物科技有限公司
ERCC1 是核苷酸切除修復(fù)通路中高度保守的切除性核酶，是有效修復(fù)烷化劑誘導(dǎo)的DNA 復(fù)合物的必要條件。研究資料表明，ERCC1 蛋白表達(dá)陰性的患者應(yīng)用順鉑輔助化療可能獲得效果良好；ERCC1 蛋白表達(dá)陽(yáng)性可能提示存在這鉑類藥物耐藥，ERCC1 可作為為患者是否應(yīng)用順鉑輔助化療的參考依據(jù)之一。
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ERCC1 人切除修復(fù)交叉互補(bǔ)基因1
【產(chǎn)品介紹】
細(xì)胞定位：細(xì)胞核
克隆號(hào)：SP68
同型：IgG
適用組織：石蠟/冰凍
陽(yáng)性對(duì)照：肺腺癌
抗原修復(fù)：熱修復(fù)（EDTA）
抗體孵育時(shí)間：30-60min
| 產(chǎn)品編號(hào) | 抗體名稱 | 克隆型別 |
| OB108 | ERCC1（人切除修復(fù)交叉互補(bǔ)基因1） | SP68 |
| OB109 | ERG | EP111 |
| OB110 | Factor Ⅷ(第八因子相關(guān)抗原) | polyclonal |
| OB111 | Factor ⅩⅢa(第十三因子a) | EP3372 |
| OB112 | FSH(卵泡刺激素) | polyclonal |
| OB113 | Galectin-3(半乳糖凝集素-3) | 9C4 |
| OB114 | GATA3（心肌轉(zhuǎn)錄因子3） | L50-823 |
| OB115 | GCDFP-15(巨囊性病液體蛋白15) | EP1582Y |
| OB116 | GFAP(膠質(zhì)纖維酸性蛋白) | EP672Y |
| OB117 | GH(生長(zhǎng)激素) | polyclonal |
| OB118 | Glucagon(胰高血糖素) | polyclonal |
| OB119 | GLUT1（葡萄糖轉(zhuǎn)化酶） | polyclonal |
| OB120 | Glycophorin A(血型糖蛋白A)或CD235a | GA-R2&HIR2 |
| OB121 | Glypican-3（磷脂酰肌醇蛋白聚糖3） | 1G12 |
| OB122 | Granzyme B(粒酶B) | polyclonal |
| OB123 | GS（谷氨酰胺合成酶） | GS-6 |
ERCC1 人切除修復(fù)交叉互補(bǔ)基因1
想了解更多的產(chǎn)品及服務(wù)請(qǐng)掃描下方二維碼：
【公司名稱】 廣州健侖生物科技有限公司
【市場(chǎng)部】 歐
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【騰訊 】
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號(hào)二期2幢101-103室
程臨釗和同事們認(rèn)為，一種解決方案就是在實(shí)驗(yàn)室中培養(yǎng)出與每個(gè)患者自身遺傳物質(zhì)相匹配，因此能夠逃避免疫系統(tǒng)的血細(xì)胞。他的研究小組已經(jīng)設(shè)計(jì)出了一種方法利用干細(xì)胞來(lái)生成人類血細(xì)胞。然而對(duì)于鐮狀細(xì)胞病患者而言有一個(gè)問(wèn)題，就是實(shí)驗(yàn)室培養(yǎng)的帶有他們遺傳物質(zhì)的干細(xì)胞同樣具有這種鐮狀細(xì)胞缺陷。為了解決這一問(wèn)題，研究人員一開(kāi)始從患者處取得血細(xì)胞，將它們編程為了誘導(dǎo)多能干細(xì)胞(iPS細(xì)胞)。
CRISPR源于包含著稱作為成簇的規(guī)律間隔的短回文重復(fù)序列(clustered regularly interspaced short palindromic repeats)DNA的片段的微生物免疫系統(tǒng)。這一工程編輯系統(tǒng)利用了一種DNA剪切酶和一段短DNA的片段，后者可將這一工具引導(dǎo)到研究人員希望在基因組中引入切口或其他改變的位置。以往的研究表明，相比于其他的基因組編輯技術(shù)例如轉(zhuǎn)錄激活樣效應(yīng)因子核酸酶(transcription activator-like effector nuclease, TALEN)，CRISPR能夠通過(guò)這些干預(yù)更有效地引起基因組改變或突變。
隨后研究人員利用這種強(qiáng)大的CRISPR技術(shù)剪掉了鐮狀細(xì)胞遺傳變異，用健康的基因版本替代了它。zui后一步就是誘導(dǎo)這些干細(xì)胞生成成熟的血細(xì)胞。研究人員發(fā)現(xiàn)，這些基因編輯干細(xì)胞能夠和未接受CRISPR處理的干細(xì)胞一樣有效地生成血細(xì)胞。
Cheng Linzhao and colleagues believe that one solution is to train in the laboratory with each patient's own genetic material to match, so to escape the immune system's blood cells. His team has devised a way to use stem cells to generate human blood cells. However, there is a problem with sickle cell disease in that laboratory-grown stem cells with their genetic material also have such sickle cell defects. To address this issue, researchers initially acquired blood cells from patients and programmed them to induce pluripotent stem cells (iPS cells).
CRISPR is derived from the microbial immune system that contains fragments of sequences known as clustered regularly interspaced short palindromic repeats. The engineering editing system uses a DNA-cleaving enzyme and a fragment of short DNA that directs the tool to the point where researchers want to introduce nicks or other changes in the genome. Previous studies have shown that CRISPR can cause genomic alterations or mutations more efficiently than these other genomic editing techniques, such as transcriptional activator-like effector nuclease (TALEN).
Researchers then used this powerful CRISPR technique to cut off the sickle cell genetic variation, replacing it with a healthy genetic version. The final step is to induce these stem cells to produce mature blood cells. The researchers found that these genetically engineered stem cells were able to produce blood cells as efficiently as stem cells that did not receive CRISPR.