EMA 上皮膜抗原

廣州健侖生物科技有限公司

EMA 是一種 400kDa 的糖蛋白，廣泛分布于各種上皮細胞及其來源的腫瘤中，分布范圍與細胞角蛋白相似，但對內(nèi)臟腺上皮的表達優(yōu)于細胞角蛋白。此抗體可與人的 EMA特異反應(yīng)，用于研究上皮及上皮源性腫瘤。EMA 陽性表達的腫瘤包括大多數(shù)的癌、間皮瘤、滑膜肉瘤和上皮樣肉瘤等，惡性淋巴瘤、黑色素瘤和軟組織腫瘤陰性表達。

近日，來自英國的科學(xué)家在生物學(xué)期刊molecular and Cellular biology在線發(fā)表了他們關(guān)于RNA聚合酶III調(diào)控巨噬細胞功能的研究進展。
研究人員指出，腫瘤微環(huán)境中的炎癥具有許多促癌癥發(fā)展效應(yīng)。特別是腫瘤相關(guān)巨噬細胞(TAM)能夠產(chǎn)生許多細胞因子，促進惡性腫瘤細胞存活，血管生成以及轉(zhuǎn)移維持腫瘤生長。腫瘤相關(guān)巨噬細胞內(nèi)細胞因子的合成與蛋白質(zhì)合成過程緊密相關(guān)，而蛋白質(zhì)的翻譯過程又依賴于RNA聚合酶III轉(zhuǎn)錄形成的眾多tRNA。因此研究RNA聚合酶III對腫瘤相關(guān)巨噬細胞的功能發(fā)揮有何影響具有重要意義。
研究人員發(fā)現(xiàn)用來源于細菌細胞壁的脂多糖(LPS)刺激小鼠巨噬細胞能夠上調(diào)表達tRNA的相關(guān)基因的轉(zhuǎn)錄。nf-kb是介導(dǎo)炎癥信號的一個關(guān)鍵轉(zhuǎn)錄因子,LPS處理能夠會增強NF-kB的p65亞基與tRNA基因的作用。除此之外，研究人員還發(fā)現(xiàn)p65能夠直接與RNA聚合酶III復(fù)合物中的轉(zhuǎn)錄因子TFIIIB相互作用，并且p65過表達會誘導(dǎo)pol III依賴性的轉(zhuǎn)錄過程。抑制巨噬細胞內(nèi)的pol III活性能夠阻止巨噬細胞分泌細胞因子并抑制其吞噬作用，這也是巨噬細胞的兩個關(guān)鍵功能特征。
這項研究揭示了RNA聚合酶III對巨噬細胞功能的重要調(diào)控作用，證明RNA聚合酶III可能對于惡性腫瘤細胞相關(guān)的免疫反應(yīng)具有重要影響。

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EMA 上皮膜抗原

【產(chǎn)品介紹】

細胞定位：細胞漿/細胞膜

克隆號：E29

同型：IgG2a/K

適用組織：石蠟/冰凍

陽性對照：直腸癌/肺腺癌

抗原修復(fù)：熱修復(fù)（EDTA）

抗體孵育時間：30-60min

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】     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號二期2幢101-103室

EMA is a 400 kDa glycoprotein that is widely distributed in a variety of epithelial cells and their origins and has a distribution similar to cytokeratin but superior to cytokeratin on gut epithelium. This antibody is specifically reactive with human EMA and is used to study epithelial and epithelial tumors. EMA-positive tumors include most cancers, mesotheliomas, synovial sarcomas and epithelioid sarcomas, etc., and negative expression in malignant lymphomas, melanomas and soft tissue tumors. Recently, scientists from the UK published their latest research progress on the regulation of macrophages by RNA polymerase III in the biology journal molecular and Cellular biology.
The researchers point out that inflammation in the tumor microenvironment has many cancer-promoting effects. In particular, tumor-associated macrophages (TAMs) are capable of producing many cytokines, promoting the survival of malignant cells, angiogenesis, and metastasis to maintain tumor growth. The synthesis of cytokines in tumor-associated macrophages is closely related to the process of protein synthesis, which in turn depends on the numerous tRNAs transcribed by RNA polymerase III. Therefore, it is important to study how RNA polymerase III affects the function of tumor-associated macrophages.
The researchers found that stimulation of mouse macrophages with lipopolysaccharide (LPS), which is derived from bacterial cell walls, can up-regulate the transcription of related genes that express tRNA. nf-kb is a key transcription factor that mediates inflammatory signaling. LPS treatment enhances the p65 subunit and tRNA genes of NF-kB. In addition, the researchers also found that p65 interacts directly with TFIIIB, a transcription factor in the RNA polymerase III complex, and overexpression of p65 induces pol III-dependent transcription. Inhibition of pol III activity in macrophages can prevent macrophages from secrete cytokines and inhibit their phagocytosis, which are two key functional features of macrophages.
This study revealed important regulatory roles of RNA polymerase III on macrophage function and demonstrated that RNA polymerase III may have important implications for the immune response associated with malignant cells.