西班牙Certest人轉鐵蛋白蛋白質（天然提取物）

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人轉鐵蛋白蛋白質（天然提取物）

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人轉鐵蛋白蛋白質（天然提取物）

這項研究成果對患有血液疾病的病人有著重大應用。科學家可以開始設計血液疾病(包括白血病)的診斷和新療法。它們將在未來的干細胞移植治療，再生醫學以及發現罕見的遺傳性血液病及免疫疾病的遺傳基礎中有著很大的價值。
美國索爾克生物研究所的科研人員發現了細胞內一個對健康老化至關重要的“開關”。這個“開關”可以促進健康細胞分裂和生長，比如，即便在衰老階段也能產生新的肺或肝組織。
在人體內，新分裂的細胞不斷補充著肺、皮膚、肝臟及其他器官。但大多數人體細胞不能無限期地分裂下去——每一次分裂后，染色體末端的細胞計時器就會縮短。當這種名為端粒的計時器變得極短時，細胞就不再分裂，導致器官和組織退化，這種現象經常發生在衰老階段。但存在一種繞過這種倒計時現象的方法：一些細胞會產生一種端粒酶，這種酶可以修復端粒，并讓細胞無限期地分裂下去。
索爾克生物研究所科研人員9月19日在《基因與發育》雜志上發表研究報告稱，他們發現端粒酶可以被關閉。
該研究報告資深作者維基·倫德布拉德教授說：“早前的研究認為端粒酶一旦聚合，在需要時可隨時利用。我們意外地發現端粒酶有一個‘關閉’開關，這個開關可以讓它分解。”
理解如何操縱這一“關閉”開關——進而延緩端粒變短的過程，可以為治療衰老性疾病帶來新方法，比如，在生命晚期再造重要的人體器官。
倫德布拉德與報告*作者、研究生蒂莫西·圖西對釀酒酵母展開了研究。早前，倫德布拉德的團隊利用這種簡單的單細胞生物體揭示了端粒酶的大量信息，并為在人體細胞中尋找類似結果奠定基礎。
圖西說：“我們本希望能夠研究端粒酶復合體的每一種成分，但事實上這并不是一項簡單的任務。”圖西制定了一套方法，可以讓他以*的分辨率觀察處于細胞生長和分裂期的每一種成分。
每當細胞分裂時，細胞的整個基因組就會被復制。當基因組進行復制時，圖西發現端粒酶在準備組合成一個復合體時，會缺失一個重要的分子亞基。但在基因組全部復制后，這個缺失的亞基會加入它的同伴中，形成一個完整的、充分活躍的端粒酶復合體。在此基礎上，端粒酶可以補充不斷磨損的染色體末端，并確保健康的細胞分裂。
但令人意外的是，圖西和倫德布拉德發現在端粒酶復合體充分組合后，它會迅速分解形成一個非活躍的“分解”復合體——事實上就是將開關調至“關閉”狀態。他們推測這種解體過程可以提供一種方式，讓端粒酶在細胞內保持極低的濃度。盡管正常細胞內不斷磨損的端粒酶會導致衰老，但癌癥細胞卻依賴提粒酶濃度，確保無節制的細胞增長。圖西和倫德布拉德發現的這個“關閉”開關可能有助于讓端粒酶的活躍度低于這一限度。

西班牙Certest人轉鐵蛋白蛋白質（天然提取物）

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

The research results have major applications in patients with blood diseases. Scientists can start designing the diagnosis and new therapies for blood diseases, including leukemia. They will be of great value in future stem cell transplantation therapies, regenerative medicine and the genetic basis for the discovery of rare hereditary blood diseases and immune diseases.
Researchers at the USS Cook Biosciences discovered a "switch" inside the cell that is vital to healthy aging. This "switch" promotes healthy cell division and growth, for example, producing new lung or liver tissue even during the aging phase.
In the body, newly dividing cells are constantly replenished with lungs, skin, liver and other organs. But most human somatic cells do not divide indefiniy - the cell timer at the end of the chromosome will be shortened after each division. When this timer called omere becomes extremely short, the cells no longer divide, resulting in the degeneration of organs and tissues, a phenomenon that often occurs during the aging phase. But there is a way to get around this countdown: Some cells produce a omerase that repairs omeres and allows cells to divide indefiniy.
Researchers at the Salk Institute for Biological Research published a study in the journal Gene and Development on September 19th saying they found that omerase can be turned off.
Professor Velen Lundbrand, senior author of the study, said: "Earlier studies suggested that omerase, once polymerized, may be readily available when needed, and we have unexpectedly found that omerase has a 'switch-off' switch It can be broken down. "
Understanding how to manipulate this "switch-off" switch, which in turn slows omere shortening, can bring new ways of treating aging diseases, such as rebuilding vital human organs in later life.
Lund Brad and the report's first author, graduate student Timothy Tucci studied Saccharomyces cerevisiae. Earlier, Lund Brad's team used this simple single-cell organism to reveal a wealth of information on omerase and laid the groundwork for finding similar results in human cells.
Tucci said: "We would have liked to study each of the components of the omerase complex, but in fact it is not a simple task." Tucci has developed a methodology that allows him to distinguish Rate observed in the cell growth and division of each component.
Every time a cell divides, the entire genome of the cell is copied. When the genome was replicating, Tucci found that omerase was missing an important molecular subunit in preparation for its assembly into a complex. But after the genome is fully replicated, this missing subunit joins its companion to form a complete and fully active omerase complex. On this basis, omerase can replenish the end of worn chromosomes and ensure healthy cell division.
Surprisingly, however, Tutsi and Lund Brad discovered that after the omerase complex has been fully assembled, it rapidly breaks down into an inactive "break down" complex - in effect switching the switch to " Disabled. They speculate that this disintegration process can provide a way for omerase to remain at very low concentrations in the cell. Although omerase, which is constantly abraded in normal cells, can cause aging, cancer cells rely on increasing omerase concentration to ensure uncontrolled cell growth. This "switch-off" switch, discovered by Tucci and Lund Brad, may help to keep omerase activity below this limit.