粘蛋白（MUC2）重組蛋白

廣州健侖生物科技有限公司

粘蛋白2是一種消化道腫瘤相關(guān)的分泌型粘蛋白，屬粘蛋白家族成員。該抗體主要表達(dá)于小腸和結(jié)腸的杯狀細(xì)胞、大部分的結(jié)腸癌和胃癌。

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粘蛋白（MUC2）重組蛋白

【產(chǎn)品介紹】

細(xì)胞定位：細(xì)胞漿

克隆號(hào)：MRQ-18

同型：IgG

適用組織：石蠟/冰凍

陽性對(duì)照：直腸/直腸癌

抗原修復(fù)：熱修復(fù)（EDTA）

抗體孵育時(shí)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(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

主要作者Richard P. Phipps博士表示：事實(shí)上，一些減肥藥包括抗抑郁藥或抗成癮藥物，并沒有在分子水平上解決脂肪細(xì)胞的堆積。盡管40年前就已經(jīng)發(fā)現(xiàn)Thy1，在其他情況下其已被研究，但它的真實(shí)分子功能卻是未知的。Phipps實(shí)驗(yàn)室*報(bào)道在脂肪細(xì)胞發(fā)育過程中Thy1表達(dá)缺失，這表明肥胖可以通過恢復(fù)Thy1來治療。
他們也正在努力開發(fā)一種抗肥胖藥物，Thy1肽，其發(fā)明已申請(qǐng)了保護(hù)。自1989年以來，Phipps一直在調(diào)查Thy1。研究的目標(biāo)是防止或減少肥胖，我們已經(jīng)展示了如何做到這一點(diǎn)的基本原則。我們相信，體重增加不一定只是吃的越來越少或鍛煉的一個(gè)結(jié)果。我們的重點(diǎn)是參與脂肪細(xì)胞發(fā)育的復(fù)雜網(wǎng)絡(luò)。
研究人員研究了小鼠和人來源的細(xì)胞系，確認(rèn)Thy1功能的缺失會(huì)促進(jìn)更多的脂肪細(xì)胞。缺乏Thy1蛋白質(zhì)小鼠、喂食高脂肪飲食后，相比于也吃相同高脂肪飲食的正常對(duì)照組小鼠，獲得了更多的重量。
Phipps和他的同事正在繼續(xù)調(diào)查為什么細(xì)胞有潛力能轉(zhuǎn)化脂肪細(xì)胞以及為什么當(dāng)Thy1關(guān)閉脂肪會(huì)積累更快。目前尚不清楚是否Thy1的水平在不同人出生時(shí)就不同，或者Thy1的水平是否由于時(shí)間發(fā)展和暴露于各種環(huán)境因素而改變。
為了解決后一個(gè)問題，Phipps實(shí)驗(yàn)室分別研究化學(xué)品即被稱為肥胖基因如雙酚A(BPA)，阻燃劑和鄰苯二甲酸鹽是否能減少人體細(xì)胞Thy1的表達(dá)，促進(jìn)肥胖。

Lead author Richard P. Phipps, PhD, said: In fact, some diet pills, including anti-depression drugs or anti-addictive drugs, did not address the accumulation of fat cells at the molecular level. Although Thy1 was discovered 40 years ago and has been studied in other contexts, its true molecular function is unknown. Phipps Laboratories first reported a loss of Thy1 expression during adipocyte development, suggesting that obesity can be treated by restoring Thy1.
They are also working to develop an anti-obesity drug, the Thy1 peptide, whose invention has been claimed for international patent protection. Phipps has been investigating Thy1 since 1989. The goal of the study is to prevent or reduce obesity, and we have demonstrated the basic principles of how to do this. We believe that weight gain is not necessarily just a consequence of eating less or exercising. Our focus is on the complex networks involved in fat cell development.
Researchers studied mouse and human-derived cell lines, confirming that loss of Thy1 function promotes more fat cells. Lack of Thy1 protein mice, after feeding a high-fat diet, gained more weight than normal control mice that also eaten the same high-fat diet.
Phipps and his colleagues are continuing to investigate why cells have the potential to transform fat cells and why fat accumulates faster when Thy1 is turned off. It is unclear whether Thy1 levels differ at birth or whether Thy1 levels change due to time development and exposure to various environmental factors.
To solve the latter problem, Phipps Laboratories separay studied whether chemicals called obesity genes such as bisphenol A (BPA), flame retardants and phthalates reduce Thy1 expression in human cells and promote obesity.