埃立克體IgG微量免疫熒光試劑盒

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：用于檢測狗血清中的埃立克體IgG抗體

產(chǎn)品規(guī)格：12 孔/張,10 張/盒

主要產(chǎn)品包括：包柔氏螺旋體菌、布魯氏菌、貝納特氏立克次體、土倫桿菌、鉤端螺旋體、新型立克次體、恙蟲病、立克次體、果氏巴貝西蟲、馬焦蟲、牛焦蟲、利什曼蟲、新包蟲、弓形蟲、貓流感病毒、貓冠狀病毒、貓皰疹病毒、犬瘟病毒、犬細小病毒等病原微生物的 IFA、MIF、ELISA試劑。

埃立克體IgG微量免疫熒光試劑盒

我司還提供其它進口或國產(chǎn)試劑盒：登革熱、瘧疾、西尼羅河、立克次體、無形體、蜱蟲、恙蟲、利什曼原蟲、RK39、漢坦病毒、深林腦炎、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。

歡迎咨詢

歡迎咨詢2042552662

二維碼掃一掃

【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號二期2幢101-3室
【企業(yè)文化】

Li發(fā)現(xiàn)，miR-17-92 的表達被鎖定在“開”的位置上的Myc依賴型癌細胞——不論是在實驗室培養(yǎng)皿中生長的還是作為腫瘤在小鼠體內(nèi)的——會不斷分裂，甚至在Myc表達被阻斷后也是如此。這提示Myc通過這個微RNA族起作用，從而施加它的致癌作用。
Li然后尋找了受到Myc過度表達影響和受到miR-17-92影響的基因的重合部分。這個研究組在這些基因中發(fā)現(xiàn)了大約401個基因同時因為Myc 和 miR-17-92而表達增加或者受到抑制。他們選擇把重點放在那些被抑制的基因上，因為這些基因表現(xiàn)出了對微RNA的平均更多的結合部位。他們進一步篩選出了被超過1個miR-17-92結合部位調(diào)控的15個基因。
在這些基因中，有5個引人注目。其中4個基因為已知調(diào)控DNA如何緊密地圍繞蛋白質(zhì)包裹起來(形成了稱為染色質(zhì)的復合體)的蛋白質(zhì)編碼。這種包裝對于讓DNA放進細胞核具有必要性，但是這讓調(diào)控轉(zhuǎn)錄的蛋白質(zhì)難以訪問基因。這4種受到Myc 和miR-17-92控制的蛋白質(zhì)通過調(diào)控這個染色質(zhì)的基因的可訪問性從而影響細胞的增殖和衰老。之前從未識別出它們是Myc 和miR-17-92的靶標。
第5個基因為一種稱為Bim的蛋白編碼，它能誘導細胞程序化死亡，即細胞凋亡。這種細胞抗原抗體路徑被身體用于清除受損或者不需要的細胞。此前有人報告說，Bim的表達受到了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胞增殖、進入細胞周期的一種休息狀態(tài)或者細胞凋亡，這部分是通過允許或禁止訪問染色質(zhì)中的緊密包裹的DNA段起作用的。
“Myc仍然是基因轉(zhuǎn)錄和表達的一個通用放大器，” Felsher說。“但是我們的研究表明癌的狀態(tài)的維持依賴于一個更專注的機制。”
zui后，Li和他的同事證明了抑制這5個目標基因的表達能有效模仿Myc過度表達，這部分緩解了Myc失去活性的影響。至多30%的培養(yǎng)的Myc依賴型癌細胞在缺乏Myc表達的情況下繼續(xù)生長(相比之下只有11%的對照細胞繼續(xù)生長)，而小鼠的腫瘤在數(shù)周時間里或者沒能消退，或者出現(xiàn)了復發(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.