Laminin 層黏連蛋白(鼠單克隆抗體)

廣州健侖生物科技有限公司

層粘連蛋白是細胞外基質的主要成分之一，腫瘤的浸潤和轉移與其遭到破壞相關。此抗體和人的層粘連蛋白反應，可用于研究基底膜，有助于研究在不同的病變過程中（如腫瘤的浸潤和轉移）基底膜所發(fā)生的變化。

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Laminin 層黏連蛋白(鼠單克隆抗體)? 

【產(chǎn)品介紹】

細胞定位：細胞漿

克隆號：LAM-89

同型：IgG

適用組織：石蠟/冰凍

陽性對照：腎臟/乳腺

抗原修復：熱修復（EDTA）

抗體孵育時間：30-60min

Laminin 層黏連蛋白(鼠單克隆抗體)

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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

論文的資深作者、科羅拉多大學醫(yī)學院生物化學和分子遺傳學教授、癌癥中心研究員James DeGregori博士說：“機體并未進化至可以應對核反應堆泄漏及CT掃描。它只能一次處理少數(shù)接受危險劑量輻射或DNA遭到其他損傷的細胞。”
DeGregori、博士生Courtney Fleenor及同事們調查了全身輻射對于小鼠造血干細胞(HSCs)的影響。在這種情況下，輻射提高了造血干細胞系統(tǒng)中的細胞發(fā)生分化的幾率。只是，雖然大多數(shù)細胞會遵循這一指令，但有少數(shù)細胞則不會。攜帶一種特異突變的干細胞能夠違抗這一分化指令，保持它們的“干性”。遺傳抑制C/EBPα 可使得少數(shù)干細胞維持這一能力，繼續(xù)充當干細胞。在與其他細胞的競爭中，健康干細胞被清除，C/EBPα 減少的干細胞在血細胞生成系統(tǒng)中占據(jù)主導地位。通過這種方式，血液系統(tǒng)從C/EBPα +細胞轉變?yōu)橹饕荂/EBPα -細胞。
導致C/EBPα 基因受到抑制的一些突變和其他遺傳變異與人類急性髓性白血病有關聯(lián)。因此，并非是輻射所引起的突變，而是被錯誤干細胞重建的血液系統(tǒng)引起了經(jīng)歷過輻射的人們的癌癥風險。
DeGregori說：“這是由自然選擇所驅動的進化。在健康血液系統(tǒng)中，健康干細胞會在競爭中勝過具有C/EBPα 突變的干細胞。但當輻射降低干細胞群的健康和適應性時，一直在那的突變細胞突然得到了接管的機會。”

"The body has not evolved to handle nuclear reactor leaks and CT scans," said senior author of the paper, Dr. James DeGregori, a professor of biochemistry and molecular genetics at the University of Colorado School of Medicine and a researcher at the Cancer Center. "It can only deal with a small number of patients receiving radiation exposure at a dangerous dose or The DNA was damaged by other cells. "
DeGregori, PhD candidate Courtney Fleenor and colleagues investigated the effects of whole body radiation on mouse hematopoietic stem cells (HSCs). In this case, radiation increases the chance of cell differentiation in the hematopoietic stem cell system. Only, although most cells follow this instruction, a few cells do not. Stem cells that carry a specific mutation are able to defy this differentiation and keep them "dry". Genetic inhibition of C / EBPα allows a small number of stem cells to maintain this capacity and continue to act as stem cells. In competition with other cells, healthy stem cells are cleared and stem cells with reduced C / EBPα dominate the hematopoietic system. In this way, the blood system changes from C / EBPα + cells to predominantly C / EBPα - cells.
Some mutations and other genetic variations that lead to the inhibition of the C / EBPα gene have been linked to human acute myeloid leukemia. Therefore, rather than the mutations caused by radiation, the blood system reconstructed by the wrong stem cells raises the cancer risk for those who have experienced radiation.
"This is evolution driven by natural selection," said DeGregori. "In a healthy blood system, healthy stem cells outperform stem cells with C / EBPα mutations in competition, but when radiation reduces the health and fitness of the stem cell population, Suddenly the mutant cells there got the chance to take over. "