WT1 腎母細(xì)胞瘤（鼠單克隆抗體）

廣州健侖生物科技有限公司

WT1是位于染色體11p13的抑癌基因，可識(shí)別間皮細(xì)胞增生、惡性間皮瘤、卵巢囊腺癌、性腺母細(xì)胞瘤、腎母細(xì)胞瘤及結(jié)締組織增生性小圓細(xì)胞腫瘤?？捎糜谘芯看俳Y(jié)締組織增生的小圓細(xì)胞瘤和Ewing肉瘤及原始神經(jīng)外胚層腫瘤。

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WT1 腎母細(xì)胞瘤（鼠單克隆抗體）

【產(chǎn)品介紹】

細(xì)胞定位：細(xì)胞核

克隆號(hào)：6F-H2

同型：IgG

適用組織：石蠟/冰凍

陽性對(duì)照：間皮瘤

抗原修復(fù)：熱修復(fù)（EDTA）

抗體孵育時(shí)間：30-60min

WT1

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【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

在這些信息的基礎(chǔ)上，我們可以同步細(xì)胞動(dòng)態(tài)，在引入轉(zhuǎn)基因時(shí)讓大多數(shù)細(xì)胞處于抗原抗體狀態(tài)。已經(jīng)有前期工作表明，重編程動(dòng)態(tài)受到一些限速步驟的調(diào)控。比如，去除組蛋白乙酰化的一個(gè)抑制子，可以使體外重編程的效率達(dá)到幾乎100%。此外，引入OSKM也會(huì)刺激甲基化等細(xì)胞過程，以維持內(nèi)穩(wěn)態(tài)。對(duì)于研究這些過程的動(dòng)態(tài)而言，定量技術(shù)將特別有優(yōu)勢(shì)。FACS和拉曼光譜才剛開始用于細(xì)胞重編程的定量研究，就已經(jīng)表現(xiàn)出了很大的潛力。
細(xì)胞重編程受到公眾關(guān)注，主要是因?yàn)樗诩膊∧M和醫(yī)療保健中的應(yīng)用。神經(jīng)退行性疾病的患者特別能從這一技術(shù)中獲益，因?yàn)樯缮窠?jīng)元的iPS方案要優(yōu)于其他細(xì)胞類型，而且患者神經(jīng)元通常很難獲取。目前，細(xì)胞重編程技術(shù)研究特定基因組突變引起的疾病，因?yàn)橹鼐幊虝?huì)重設(shè)表觀基因組。盡管有證據(jù)表明，iPS技術(shù)也能用來研究復(fù)雜基因組改變引起的疾病，但目前的模型一般不足以研究異常細(xì)胞網(wǎng)絡(luò)或動(dòng)態(tài)引發(fā)的疾病。

Based on this information, we can synchronize cellular dynamics, allowing most cells to be in an antigen-antibody state upon introduction of the transgene. Preliminary work has shown that reprogramming is dynamically limited by some rate-limiting steps. For example, removing a suppressor of histone acetylation can make reprogramming nearly 100% efficient in vitro. In addition, the introduction of OSKM also stimulates cellular processes such as methylation to maintain homeostasis. Quantitative techniques will be particularly advantageous for studying the dynamics of these processes. FACS and Raman spectroscopy have just begun to be used in quantitative studies of cell reprogramming and have shown great potential.
Cell reprogramming has received public attention primarily because of its use in disease simulation and healthcare. In particular, patients with neurodegenerative diseases benefit from this technique because the iPS regimen that produces neurons is superior to other cell types and is often difficult to obtain in patient neurons. Currently, cell reprogramming is best suited to study diseases caused by specific genomic mutations because reprogramming resets the epigenome. Although there is evidence that iPS technology can also be used to study diseases caused by complex genome changes, current models are generally not adequate for studying abnormal cell networks or dynamically induced diseases.