埃立克体IgG微量免疫荧光试剂盒

Ehrlichia canis Canine IFA IgG Kit

广州健仑生物科技有限公司

主要用途：用于检测狗血清中的埃立克体IgG抗体

产品规格：12 孔/张,10 张/盒

主要产品包括：包柔氏螺旋体菌、布鲁氏菌、贝纳特氏立克次体、土伦杆菌、钩端螺旋体、新型立克次体、恙虫病、立克次体、果氏巴贝西虫、马焦虫、牛焦虫、利什曼虫、新包虫、弓形虫、猫流感病毒、猫冠状病毒、猫疱疹病毒、犬瘟病毒、犬细小病毒等病原微生物的 IFA、MIF、ELISA试剂。

埃立克体IgG微量免疫荧光试剂盒

我司还提供其它进口或国产试剂盒：登革热、疟疾、西尼罗河、立克次体、无形体、蜱虫、恙虫、利什曼原虫、RK39、汉坦病毒、深林脑炎、流感、A链球菌、合胞病毒、腮病毒、乙脑、寨卡、黄热病、基孔肯雅热、克锥虫病、违禁品滥用、肺炎球菌、军团菌、化妆品检测、食品安全检测等试剂盒以及日本生研细菌分型诊断血清、德国SiFin诊断血清、丹麦SSI诊断血清等产品。

欢迎咨询

欢迎咨询2042552662

二维码扫一扫

【公司名称】 广州健仑生物科技有限公司
【】    杨永汉 
【】 
【腾讯 】 2042552662
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-3室
【企业文化】

Li发现，miR-17-92 的表达被锁定在“开”的位置上的Myc依赖型癌细胞——不论是在实验室培养皿中生长的还是作为肿瘤在小鼠体内的——会不断分裂，甚至在Myc表达被阻断后也是如此。这提示Myc通过这个微RNA族起作用，从而施加它的致癌作用。
Li然后寻找了受到Myc过度表达影响和受到miR-17-92影响的基因的重合部分。这个研究组在这些基因中发现了大约401个基因同时因为Myc 和 miR-17-92而表达增加或者受到抑制。他们选择把重点放在那些被抑制的基因上，因为这些基因表现出了对微RNA的平均更多的结合部位。他们进一步筛选出了被超过1个miR-17-92结合部位调控的15个基因。
在这些基因中，有5个引人注目。其中4个基因为已知调控DNA如何紧密地围绕蛋白质包裹起来(形成了称为染色质的复合体)的蛋白质编码。这种包装对于让DNA放进细胞核具有必要性，但是这让调控转录的蛋白质难以访问基因。这4种受到Myc 和miR-17-92控制的蛋白质通过调控这个染色质的基因的可访问性从而影响细胞的增殖和衰老。之前从未识别出它们是Myc 和miR-17-92的靶标。
第5个基因为一种称为Bim的蛋白编码，它能诱导细胞程序化死亡，即细胞凋亡。这种细胞抗原抗体路径被身体用于清除受损或者不需要的细胞。此前有人报告说，Bim的表达受到了miR-17-92的影响。
值得注意的是，所有这些蛋白已知都能影响细胞增殖、进入细胞周期的一种休息状态或者细胞凋亡，这部分是通过允许或禁止访问染色质中的紧密包裹的DNA段起作用的。
“Myc仍然是基因转录和表达的一个通用放大器，” Felsher说。“但是我们的研究表明癌的状态的维持依赖于一个更专注的机制。”
zui后，Li和他的同事证明了抑制这5个目标基因的表达能有效模仿Myc过度表达，这部分缓解了Myc失去活性的影响。至多30%的培养的Myc依赖型癌细胞在缺乏Myc表达的情况下继续生长(相比之下只有11%的对照细胞继续生长)，而小鼠的肿瘤在数周时间里或者没能消退，或者出现了复发。

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.