埃立克體IgG微量免疫熒光試劑盒

Ehrlichia canis Canine IFA IgG Kit

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)狗血清中的埃立克體IgG抗體

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埃立克體IgG微量免疫熒光試劑盒

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【公司名稱(chēng)】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
【騰訊 】 2042552662
【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101-3室
【企業(yè)文化】

Li發(fā)現(xiàn)，miR-17-92 的表達(dá)被鎖定在“開(kāi)”的位置上的Myc依賴(lài)型癌細(xì)胞——不論是在實(shí)驗(yàn)室培養(yǎng)皿中生長(zhǎng)的還是作為腫瘤在小鼠體內(nèi)的——會(huì)不斷分裂，甚至在Myc表達(dá)被阻斷后也是如此。這提示Myc通過(guò)這個(gè)微RNA族起作用，從而施加它的致癌作用。
Li然后尋找了受到Myc過(guò)度表達(dá)影響和受到miR-17-92影響的基因的重合部分。這個(gè)研究組在這些基因中發(fā)現(xiàn)了大約401個(gè)基因同時(shí)因?yàn)镸yc 和 miR-17-92而表達(dá)增加或者受到抑制。他們選擇把重點(diǎn)放在那些被抑制的基因上，因?yàn)檫@些基因表現(xiàn)出了對(duì)微RNA的平均更多的結(jié)合部位。他們進(jìn)一步篩選出了被超過(guò)1個(gè)miR-17-92結(jié)合部位調(diào)控的15個(gè)基因。
在這些基因中，有5個(gè)引人注目。其中4個(gè)基因?yàn)橐阎{(diào)控DNA如何緊密地圍繞蛋白質(zhì)包裹起來(lái)(形成了稱(chēng)為染色質(zhì)的復(fù)合體)的蛋白質(zhì)編碼。這種包裝對(duì)于讓DNA放進(jìn)細(xì)胞核具有必要性，但是這讓調(diào)控轉(zhuǎn)錄的蛋白質(zhì)難以訪問(wèn)基因。這4種受到Myc 和miR-17-92控制的蛋白質(zhì)通過(guò)調(diào)控這個(gè)染色質(zhì)的基因的可訪問(wèn)性從而影響細(xì)胞的增殖和衰老。之前從未識(shí)別出它們是Myc 和miR-17-92的靶標(biāo)。
第5個(gè)基因?yàn)橐环N稱(chēng)為Bim的蛋白編碼，它能誘導(dǎo)細(xì)胞程序化死亡，即細(xì)胞凋亡。這種細(xì)胞抗原抗體路徑被身體用于清除受損或者不需要的細(xì)胞。此前有人報(bào)告說(shuō)，Bim的表達(dá)受到了miR-17-92的影響。
值得注意的是，所有這些蛋白已知都能影響細(xì)胞增殖、進(jìn)入細(xì)胞周期的一種休息狀態(tài)或者細(xì)胞凋亡，這部分是通過(guò)允許或禁止訪問(wèn)染色質(zhì)中的緊密包裹的DNA段起作用的。
“Myc仍然是基因轉(zhuǎn)錄和表達(dá)的一個(gè)通用放大器，” Felsher說(shuō)。“但是我們的研究表明癌的狀態(tài)的維持依賴(lài)于一個(gè)更專(zhuān)注的機(jī)制。”
zui后，Li和他的同事證明了抑制這5個(gè)目標(biāo)基因的表達(dá)能有效模仿Myc過(guò)度表達(dá)，這部分緩解了Myc失去活性的影響。至多30%的培養(yǎng)的Myc依賴(lài)型癌細(xì)胞在缺乏Myc表達(dá)的情況下繼續(xù)生長(zhǎng)(相比之下只有11%的對(duì)照細(xì)胞繼續(xù)生長(zhǎng))，而小鼠的腫瘤在數(shù)周時(shí)間里或者沒(méi)能消退，或者出現(xiàn)了復(fù)發(fā)。

Li found that Myc-dependent cancer cells, whose expression of miR-17-92 is locked in the "on" position, either in a lab dish or as a tumor in a mouse, continue to divide , Even after Myc expression was blocked. This suggests that Myc acts through this microRNA family, exerting its oncogenic role.
Li then looked for a coincidence of genes that were affected by Myc overexpression and affected by miR-17-92. In the study group, about 401 genes were found in these genes to be increased or inhibited by both Myc and miR-17-92. They chose to focus on those genes that were suppressed because these genes showed an even greater number of binding sites for microRNAs. They further screened 15 genes that are regulated by more than one miR-17-92 binding site.
Five of these genes attract attention. Four of these genes are known as proteins that regulate how DNA binds tightly around a protein that forms a complex called the chromatin. This packaging is necessary to put DNA into the nucleus, but it makes it hard to access genes that regulate the transcription of proteins. These four proteins, controlled by Myc and miR-17-92, affect the proliferation and senescence of cells by regulating the accessibility of this chromatin gene. They were never previously identified as targets of Myc and miR-17-92.
The fifth gene, a protein called Bim, codes for programmed cell death, apoptosis. This cellular antigen-antibody pathway is used by the body to clear damaged or unwanted cells. Earlier it was reported that Bim expression was affected by miR-17-92.
It is noteworthy that all of these proteins are known to affect cell proliferation, into a resting state of the cell cycle or apoptosis, in part by allowing or disabling access to tightly wrapped DNA segments in chromatin.
"Myc is still a universal amplifier for gene transcription and expression," Felsher said. "But our research shows that the maintenance of cancer status depends on a more focused mechanism."
Finally, Li and his colleagues demonstrated that inhibition of the expression of these five target genes mimics Myc overexpression, partially alleviating the effects of Myc loss of activity. Up to 30% of cultured Myc-dependent cancer cells continue to grow in the absence of Myc expression (compared with only 11% of control cells continue to grow), whereas the tumor in mice fails or does not regress in weeks, Or there is a recurrence.