果氏巴貝西蟲IgM免疫熒光試劑盒

Babesia microti IgM IFA Kit

廣州健侖生物科技有限公司

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果氏巴貝西蟲IgM免疫熒光試劑盒

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【公司名稱】 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
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美國斯坦福大學(xué)醫(yī)學(xué)院的科研人員發(fā)現(xiàn)，這種稱為Myc的蛋白質(zhì)通過一種稱為微RNA的微小的調(diào)控分子起作用，抑制這些基因的表達(dá)。這標(biāo)志著Myc控制的基因的一個(gè)子集*被發(fā)現(xiàn)是這種蛋白質(zhì)的致癌功能的關(guān)鍵參與者，并且提示了對(duì)于Myc依賴型癌癥的新的治療靶標(biāo)。
“這是思考微RNA以及染色質(zhì)包裝在癌癥中的作用的一種不同的方式，”這項(xiàng)研究的*作者、醫(yī)學(xué)博士、理學(xué)博士、腫瘤學(xué)與病理學(xué)教授Dean Felsher說。“我們非常吃驚地發(fā)現(xiàn)一種微RNA的過度表達(dá)可能模仿Myc的致癌效應(yīng)。”*作者是該校教師、醫(yī)學(xué)博士、理學(xué)博士Yulin Li。
這組科研人員識(shí)別出的這些基因制造蛋白質(zhì)從而管理細(xì)胞通過分裂進(jìn)行自我更新、進(jìn)入一種稱為衰老的休息狀態(tài)，或者通過細(xì)胞程序化抗原抗體永遠(yuǎn)退役。這些過程的精細(xì)控制對(duì)于控制或清除可能危險(xiǎn)的腫瘤細(xì)胞是必要的。
為Myc蛋白編碼的基因是有名的強(qiáng)致癌基因——致癌基因是用于描述突變或不正常表達(dá)的時(shí)候會(huì)導(dǎo)致癌癥的基因的一個(gè)術(shù)語。它調(diào)控著一個(gè)細(xì)胞的大約1萬個(gè)基因和微RNA的表達(dá)?？茖W(xué)家長(zhǎng)久以來知道，讓Myc失去活性或者阻斷它的表達(dá)，能夠?qū)е乱蕾嘙yc的癌細(xì)胞停止生長(zhǎng)或死亡，還會(huì)導(dǎo)致患Myc依賴型實(shí)體癌的小鼠的腫瘤消退。這種依賴現(xiàn)象稱為癌基因成癮。
微RNA是小型的RNA分子(只有大約22個(gè)核苷酸)，它和Myc一樣，可以調(diào)控基因表達(dá)。此前的研究已經(jīng)證明了Myc過度表達(dá)導(dǎo)致了稱為miR-17-92的一族微RNA的水平增加。
“多年來人們已經(jīng)知道m(xù)yc調(diào)控著微RNA的表達(dá)，” Felsher說。“但是不清楚這與Myc的致癌功能的關(guān)系是怎樣的。”

Researchers at the Stanford University School of Medicine in the United States found that this protein, known as Myc, acts through tiny regulatory molecules called microRNAs that suppress the expression of these genes. This marks the first time that a subset of Myc-controlled genes has been found to be a key player in the oncogenic function of this protein and suggests new therapeutic targets for Myc-dependent cancers.
"This is a different way of thinking about the role of microRNAs and chromatin packaging in cancer," said Dean Felsher, a senior author of the study, MD, PhD, professor of oncology and pathology. "We were very surprised to find that overexpression of a microRNA might mimic Myc's oncogenic effect." The lead author was Yulin Li, MD, Ph.D., the school's teacher.
The genes identified by the group of researchers make proteins that governs cell self-renewal by cleavage, into a state of rest called aging, or permanent retiring by a programmed antigen-antibody. Fine control of these processes is necessary to control or eliminate potentially dangerous tumor cells.
The gene that codes for Myc protein is a well-known strong oncogene - an oncogene is a term used to describe a gene that causes cancer when mutated or abnormally expressed. It regulates the expression of about 10,000 genes and microRNAs in a cell. Scientists have long known that inactivating Myc or blocking its expression can cause Myc-dependent cancer cells to stop growing or die, as well as tumor regression in mice with Myc-dependent solid cancers. This phenomenon of dependence is called oncogene addiction.
MicroRNAs are small RNA molecules (only about 22 nucleotides in length) that, like Myc, regulate gene expression. Previous studies have demonstrated that Myc overexpression leads to increased levels of a family of microRNAs called miR-17-92.
"It has been known for years that myc regulates microRNA expression," Felsher said. "But it is unclear what the relationship is with Myc's oncogenic function."