西班牙Certest彎曲桿菌重組外膜蛋白

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彎曲桿菌重組外膜蛋白

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西班牙Certest彎曲桿菌重組外膜蛋白

Lauren Hirao說：“了解免疫反應中的參與因子，對于開發新的治療方法非常重要。弄清這些事件如何發展，能夠幫助我們發現干預的zui恰當時機。”
姜黃素是姜黃的活性成分，已被科學研究用于許多類型癌癥的治療。姜黃素已被證明具有癌化學預防作用，能扭轉，抑制或阻止癌癥發展的能力。
磷酸化負責開啟和關閉蛋白質，改變蛋白質的功能和活性。皮層蛋白過度磷酸化活化已與癌癥侵略性密切相關。亞利桑那州大學的研究人員用姜黃素處理結腸癌細胞發現，姜黃素能關閉皮層蛋白的活性形式，因此，當皮層蛋白被關閉時，癌細胞失去移動能力，并且不能轉移到身體的其他部分。
更具體地說，姜黃素通過與皮層蛋白相互作用，并激活PTPN1酶，“關閉”皮層蛋白。PTPN1酶作為一種磷酸酶，可從皮層蛋白中去除磷酸基團，也即“去磷酸化”過程。而皮層蛋白去磷酸化與結腸癌細胞遷移能力降低相關。
通過確定姜黃素激活酶PTPN1，然后關閉皮層蛋白的活性部位pTyr421，研究人員認為其可以開發成針對癌細胞皮層蛋白的化學預防藥物，以防止癌癥的轉移性。
ALK7受體主要發現在脂肪細胞和參與調控代謝的組織中。有趣的是，ALK7突變小鼠的脂肪積累比攜帶一個功能版本蛋白質的小鼠還要少。到現在為止，人們還不清楚為什么會這樣。
研究人員構建了脂肪細胞缺乏ALK7，但是其他細胞都能夠正常產生ALK7的小鼠。研究人員發現，缺乏ALK7受體的脂肪細胞對腎上腺素和去甲腎上腺素信號更加敏感，這一發現解釋了，為何這些小鼠積累的脂肪更少，即使這些小鼠被喂食高脂肪飲食。腎上腺素和去甲腎上腺素是新陳代謝的關鍵因子。這些激素引發能量爆發，并加快心臟速率以及血壓升高，這些都是對“戰或逃”激素的必需應答。
這些激素通常刺激脂肪的分解，但是當營養物質很豐富時，脂肪細胞就會對這個信號產生抗性，從而儲存脂肪。這一機制在食物供應豐富時轉變為有利于能量儲存，從而提高饑餓時的生存率。在工業化國家，食物經常供應不斷，這種阻力可能會導致體內脂肪不健康的增加，進而導致肥胖癥。
然后，研究人員研究了，阻止ALK7是否能夠防止肥胖。目前，還沒有已知的ALK7抑制劑，但研究人員利用小鼠生成ALK7的一個特殊突變體，使得它通過化學物質來抑制敏感，從而解決了上述的問題。這有可能實現作者能夠在任何時間阻斷其它正常成年動物的受體。
“使用這種方法，我們可以通過化學物質的簡單調控，使得高脂肪飲食小鼠變瘦。這表明，ALK7受體的急性抑制可預防成年動物的肥胖，”神經科學系和這項研究的*作者 Tingqing Guo說。

西班牙Certest彎曲桿菌重組外膜蛋白

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【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

"Understanding the factors involved in the immune response is important for developing new treatments," explains Lauren Hirao, and figuring out how these events have evolved helps us find the right time to intervene. "
Curcumin, the active ingredient of turmeric, has been scientifically used in the treatment of many types of cancer. Curcumin has been shown to have a chemopreventive effect on cancer that can reverse, inhibit or prevent the development of cancer.
Phosphorylation is responsible for turning proteins on and off, altering the function and activity of the protein. Over-phosphorylation of cortical proteins has been implicated in cancer aggressiveness. Using curcumin to treat colon cancer cells, researchers at the University of Arizona found that curcumin can turn off the active form of cortical proteins, so that when cortical proteins are switched off, cancerous cells lose their ability to move and can not be transferred to other parts of the body.
More specifically, curcumin "closes" the cortex protein by interacting with cortical proteins and activating the PTPNl enzyme. The PTPN1 enzyme, a phosphatase that removes phosphate groups from the cortex protein, is also known as the "dephosphorylation" process. Dephosphorylation of cortical proteins is associated with decreased colon cell migration.
By identifying the curcumin-activating enzyme, PTPN1, and then shutting down the active site of cortical protein, pTyr421, researchers believe it could be developed as a chemopreventive drug against cancer cell cortex proteins to prevent cancer metastasis.
ALK7 receptors are mainly found in adipocytes and tissues involved in the regulation of metabolism. Interestingly, ALK7 mutant mice have less fat accumulation than mice that carry a functional version of the protein. Until now, it is unclear why this is so.
The researchers constructed mice that lacked ALK7 in their fat cells, but all other cells were able to produce ALK7 normally. The researchers found that adipocytes lacking the ALK7 receptor are more sensitive to epinephrine and norepinephrine signaling, a finding that explains why these mice accumulate less fat, even though these mice are fed a high-fat diet. Epinephrine and norepinephrine are the key metabolic factors. These hormones trigger an energy burst and speed up the heart rate and blood pressure, which are all necessary responses to "war or escape" hormones.
These hormones usually stimulate the breakdown of fat, but when the nutrients are plentiful, fat cells resist the signal and store fat. This mechanism transforms into beneficial energy storage when food supplies are abundant, thereby increasing the survival rate in starvation. In industrialized countries, where food is regularly supplied, this resistance can lead to an unhealthy increase in body fat which can lead to obesity.
Then, the researchers studied whether preventing ALK7 could prevent obesity. There are no known inhibitors of ALK7, but researchers have used mice to generate a particular mutant of ALK7 that makes it immune to chemicals by chemicals that solve the problems described above. This makes it possible for the author to block the receptors of other normal adult animals at any time.
"By using this method, we can make mice with high-fat diet thin by simple chemical regulation, suggesting that acute inhibition of ALK7 receptors may prevent obesity in adult animals," the Department of Neuroscience and the One author, Tingqing Guo said.