西班牙Certest肺炎鏈球菌單克隆抗體(克隆SN3)

廣州健侖生物科技有限公司

廣州健侖長期供應各種生物原料，主要代理品牌：西班牙Certest。

主要產品包括各種生物單克隆抗原抗體、重組蛋白。

西班牙 Certest肺炎鏈球菌單克隆抗體(克隆SN3)

我司還提供其它進口或國產試劑盒：登革熱、瘧疾、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診斷血清等產品。

歡迎咨詢

歡迎咨詢2042552662

【產品介紹】

西班牙 Certest肺炎鏈球菌單克隆抗體(克隆SN3)

近日，來自英國的科學家在生物學期刊molecular and Cellular biology在線發表了他們關于RNA聚合酶III調控巨噬細胞功能的研究進展。
研究人員指出，腫瘤微環境中的炎癥具有許多促癌癥發展效應。特別是腫瘤相關巨噬細胞(TAM)能夠產生許多細胞因子，促進惡性腫瘤細胞存活，血管生成以及轉移維持腫瘤生長。腫瘤相關巨噬細胞內細胞因子的合成與蛋白質合成過程緊密相關，而蛋白質的翻譯過程又依賴于RNA聚合酶III轉錄形成的眾多tRNA。因此研究RNA聚合酶III對腫瘤相關巨噬細胞的功能發揮有何影響具有重要意義。
研究人員發現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表達tRNA的相關基因的轉錄。nf-kb是介導炎癥信號的一個關鍵轉錄因子,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，研究人員還發現p65能夠直接與RNA聚合酶III復合物中的轉錄因子TFIIIB相互作用，并且p65過表達會誘導pol III依賴性的轉錄過程。抑制巨噬細胞內的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控作用，證明RNA聚合酶III可能對于惡性腫瘤細胞相關的免疫反應具有重要影響。
干細胞可以轉變為任何類型的細胞，科學家們一直渴望把這種“超能力”利用起來。不過，這種“超能力”在癌癥治療中又是一個令人擔憂的問題。人們認為，惡性腫瘤中的干細胞能幫助癌癥抵抗治療。zui近一項新研究表明，癌癥干細胞的威脅超乎人們的想象。
在此之前，人們只在快速生長的侵襲性腫瘤中鑒定到干細胞。但華盛頓大學的研究團隊在小鼠模型中發現，緩慢生長的腫瘤也擁有令人頭疼的干細胞。而且這些低級別癌癥干細胞對抗癌藥物很不敏感，這項研究發表在三月十二日的Cell Reports雜志上。
研究人員將這些癌癥干細胞與健康干細胞進行了比較，發現了它們抵抗藥物治療的機制，并由此提出了新的治療策略。“我們需要加大藥物劑量或者使用不同的藥物，以確保殺死這些癌癥干細胞，”文章的資深作者，華盛頓大學的David H. Gutmann教授說。*作者Yi-Hsien Chen博士建立了NF1型低級別腦瘤的小鼠模型。他在小鼠模型中鑒定了癌癥干細胞，并且證明這些細胞移植到正常小鼠中能夠形成腫瘤。

西班牙 Certest肺炎鏈球菌單克隆抗體(克隆SN3)

想了解更多的產品及服務請掃描下方二維碼：

【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

【】 
【騰訊  】 2042552662
【公司地址】 廣州清華科技園創新基地番禺石樓鎮創啟路63號二期2幢101-103室

Recently, scientists from the UK published their latest online research on molecular 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 characteristics 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.
Stem cells can be transformed into any type of cell, scientists have been eager to use this "super power." However, this "super power" is another worry in cancer treatment. It is believed that stem cells in malignancies can help treat cancer resistance. A recent new study shows that the threat of cancer stem cells beyond the imagination of people.
Previously, stem cells were identified only in rapidly growing aggressive tumors. But a team from the University of Washington found in the mouse model that slow-growing tumors also have troublesome stem cells. And these low-grade cancer stem cells are not sensitive to anticancer drugs, the study was published in the March 12 issue of Cell Reports.
The researchers compared these cancer stem cells with healthy stem cells and found that they were resistant to drug treatment mechanisms and came up with new treatment strategies. "We need to increase drug doses or use different drugs to make sure we kill these cancer stem cells," said David H. Gutmann, a professor at the University of Washington who is a senior author of the article. The first author, Yi-Hsien Chen, Ph.D., established a mouse model of NF1-type low-grade brain tumor. He identified cancer stem cells in a mouse model and demonstrated that these cells transplanted into normal mice were able to form tumors.