詳細(xì)介紹
Renal Cell Carcinoma Marker 腎細(xì)胞癌標(biāo)記
廣州健侖生物科技有限公司
RCC在90%以上原發(fā)性腎細(xì)胞癌、 80%左右轉(zhuǎn)移性腎細(xì)胞癌陽性表達(dá)。與CD10可聯(lián)合用于轉(zhuǎn)移性腎細(xì)胞癌的研究。RCC還表達(dá)于乳腺腺泡和導(dǎo)管上皮細(xì)胞的腔面、附睪上皮細(xì)胞及甲狀旁腺主細(xì)胞內(nèi)、甲狀腺濾泡內(nèi)的膠質(zhì)。
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Renal Cell Carcinoma Marker 腎細(xì)胞癌標(biāo)記
【產(chǎn)品介紹】
細(xì)胞定位:細(xì)胞漿/細(xì)胞膜
克隆號:66.4.C2
同型:IgG
適用組織:石蠟/冰凍
陽性對照:腎細(xì)胞癌/正常腎
抗原修復(fù):熱修復(fù)(EDTA)
抗體孵育時間:30-60min
產(chǎn)品編號 | 抗體名稱 | 克隆型別 |
OB217 | PTEN (10號染色體缺失磷酸酶及張力蛋白同源基因) | polyclonal |
OB218 | PTH試劑(甲狀旁腺素) | MRQ-31 |
OB219 | PU.1(Ets蛋白轉(zhuǎn)錄因子) | EPR3158Y |
OB220 | RCC(Renal Cell Carcinoma Marker)(腎細(xì)胞癌標(biāo)記) | 66.4.C2 |
OB221 | S100P(S100P蛋白) | 16/f5 |
OB222 | S-100(S-100蛋白) | 4C4.9 |
OB223 | SALL4(SALL4蛋白) | 6E3 |
OB224 | Smoothelin(平滑肌細(xì)胞特異性抗原) | R4A |
OB225 | SOX-10試劑(Sry相關(guān)HMG-Box基因10) | EP268 |
OB226 | SOX-11(Sry相關(guān)HMG-Box基因11) | MRQ-58 |
OB227 | SOX-2試劑(Sry相關(guān)HMG-Box基因2) | SP76 |
OB228 | Stathmin試劑(微管解聚蛋白) | SP49 |
OB229 | Surfactant(表面活性蛋白)或SP-B(Surfactant Protein B) | 1B9 |
OB230 | Survivin(存活蛋白) | EP119 |
OB231 | Synaptophysin(突觸素) | MRQ-40 |
OB232 | TAG-72(腫瘤相關(guān)糖蛋白) | B72.3 |
OB233 | Tau試劑(Tau蛋白) | polyclonal |
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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
近日,來自牛津大學(xué)的科學(xué)家通過研究,揭示了控制機體上皮細(xì)胞形狀和運動狀態(tài)發(fā)生轉(zhuǎn)變的關(guān)鍵機制,相關(guān)研究刊登于雜志Nature Cell biology上;文章中研究者表示,名為ASPP2的腫瘤抑制蛋白的功能就好比是一種分子開關(guān),其可以控制并且逆轉(zhuǎn)機體上皮細(xì)胞的形狀及運動狀態(tài)的改變,這對于解釋一系列生化現(xiàn)象,比如傷口愈合、胚胎發(fā)育及癌癥轉(zhuǎn)移都非常關(guān)鍵。
研究者Xin Lu表示,目前我們盡力去鑒別出控制控制上皮細(xì)胞可塑性的分子開關(guān),這樣的可塑性是癌癥的標(biāo)志,為了發(fā)生轉(zhuǎn)移,癌細(xì)胞會疏松自身的結(jié)構(gòu),不斷擺動脫離母體腫瘤組織,進而在機體其它組織器官部位“安家”,上述的過程就稱為上皮細(xì)胞向間充質(zhì)細(xì)胞的轉(zhuǎn)分化過程及間質(zhì)細(xì)胞向上皮細(xì)胞的轉(zhuǎn)化過程(EMT及MET)。
研究者發(fā)現(xiàn),在腎小管的發(fā)育過程中ASPP2蛋白會促使MET過程的發(fā)生,從而過濾掉機體血液中的廢棄物,而當(dāng)ASPP2蛋白缺失時會促進EMT過程的發(fā)生,尤其是在表達(dá)常見癌癥基因RAS細(xì)胞中,EMT過程尤為明顯,從而就會引發(fā)癌癥發(fā)生轉(zhuǎn)移。隨后研究人員對小鼠模型進行試驗發(fā)現(xiàn),當(dāng)小鼠機體中抗原抗體癌細(xì)胞表達(dá)較低水平的ASPP2時,其就會大量轉(zhuǎn)移至大腦細(xì)胞中,如果這些抗原抗體癌細(xì)胞表達(dá)較足量的ASPP2,其轉(zhuǎn)移的能力就會明顯下降。
Recently, scientists from Oxford University revealed the key mechanisms that control the change of the epithelial cell shape and movement in the body. Relevant research is published in the journal Nature Cell Biology. In the article, researchers said that the tumor suppressor protein called ASPP2 Is like a molecular switch that controls and reverses changes in the shape and motility of the body's epithelium, which is crucial for interpreting a range of biochemical phenomena such as wound healing, embryonic development, and cancer metastasis.
Xin Lu, a researcher, said that at present we try our best to identify molecular switches that control the plasticity of epithelial cells. Such plasticity is a hallmark of cancer. In order to metastasize, cancerous cells loose their structure and constantly swing away from the mother's tumor tissue, Other parts of the body organs "home", the above process is called the epithelial cells to mesenchymal cells transdifferentiation process and the conversion of stromal cells to epithelial cells (EMT and MET).
The researchers found that during the development of tubules, ASPP2 protein can promote the occurrence of MET process and thus filter out the body's blood waste, and when ASPP2 protein is missing, it can promote EMT process, especially in the expression of common cancer genes RAS cells, the EMT process is particularly evident, which will trigger the transfer of cancer. Subsequently, researchers conducted experiments on mouse models and found that when the antigen-antibody-expressing cancer cells in the mouse body express a lower level of ASPP2, they can be largely transferred to the brain cells. If these antigen-antibody-expressing cancer cells express a sufficient amount of ASPP2 , Its ability to transfer will be significantly reduced.