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首先作者以普通大鼠腎臟細胞為研究對象，發現這些細胞在遷移的過程中會不斷地向胞外釋放內容物，這種新發現的細胞事件被稱為遷移胞吐作用(migracytosis)。細胞在遷移的過程中會將其收縮纖維留在胞體后側。在收縮纖維的橫截面處會有很多直徑約為3um的囊泡，即為新發現的"遷移小體"。這些遷移小體中還包括有很多直徑約50~100nm的小泡。zui終收縮纖維會發生斷裂，從而這些遷移小體會釋放到胞外并被周圍的細胞吞噬。
由于之前沒有任何相關的報道，為了進一步研究，需要進行純化。作者通過密度梯度離心的方法得到了細胞裂解物的不同組分，比較發現migrasome富集在某一特定的組分中。之后，作者通過質譜的手段篩選了一系列migrasome特異性的蛋白，在大量膜蛋白與細胞骨架相關蛋白的候選物中，作者發現Tetraspanin-4(TSPAN4)是其中migrasome定位zui準確的蛋白質，因此作者人工構建了(TSPAN4)-熒光報告基因供后續研究。進一步研究發現：當細胞密度很大時，TSPAN4在細胞內的分布十分彌散，只有在細胞膜上有少量富集;但是當細胞密度較低時，隨著細胞收縮纖維的伸長，很多TSPAN4富集于收縮纖維區域，特別是其表面的環狀結構。之后，作者通過比較共聚焦顯微鏡成像結果與電鏡投射結果，證實了這部分"環狀"的結構即之前發現的migrasome。
之后，作者通過一系列藥物處理，發現migrasome的形成依賴于細胞的遷移過程，而且依賴于細胞骨架蛋白actin的多聚化。另外，體外過表達的實驗與對動物組織的檢測分別證明migrasome在各類細胞系以及原代細胞中是廣泛存在的。
zui后作者發現在細胞遷移過程中，胞體持續地向migrasome中運輸胞內物質。當細胞釋放migrasome后，這些囊泡會被周圍的細胞所吞噬。
綜上，作者通過一系列的生化手段證明了他們發現的一類新的亞細胞結構-"遷移小體"。它在細胞遷移中的作用雖然還未知，但這一過程明顯影響了細胞間的通訊。這一發現對經典的細胞生物學得到了補充。
近日，生物學期刊Cell death &differentiation刊登了來自德克薩斯大學休斯敦健康科學中心MG Kolonin研究小組的一項研究成果，他們利用hunter-killer peptide選擇性誘導白色脂肪前體細胞發生細胞凋亡，結果發現在高脂誘導肥胖模型中，白色脂肪生長受到抑制，同時發現脂肪組織中米色脂肪細胞出現代償性增加，這或許可以為我們靶向白色脂肪前體細胞，調控白色脂肪代謝活性，治療肥胖提供一種策略。

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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

First of all, the author used ordinary rat kidney cells as the research object and found that these cells continuously release the contents to the outside during the process of migration. The newly discovered cell event is called migracytosis. Cells migrate their contractile fibers to the back of the cell body during migration. There are many vesicles about 3um in diameter at the cross-section of the deflated fiber, the newly discovered "migrating bodies." These migration bodies also include many small bubbles about 50 ~ 100nm in diameter. The final defibrillated fibers break and the migrating bodies release to the extracellular and are swallowed by the surrounding cells.
Since there was no previous report, for further study, purification was required. The authors obtained different components of cell lysates by density gradient centrifugation, and found that migrasome is enriched in a particular component. After that, the authors screened a series of migrasome-specific proteins by mass spectrometry. In a large number of candidates for membrane proteins and cytoskeleton-associated proteins, the authors found that Tetraspanin-4 (TSPAN4) is the most accurate protein in which migrasome is located, The (TSPAN4) -fluorescent reporter gene was constructed manually for later study. Further studies showed that when the cell density is very high, the distribution of TSPAN4 in the cell is very diffuse, and only a small amount of enrichment is found in the cell membrane. However, when the cell density is low, many TSPAN4 are enriched with the cell shrinkage fiber elongation In the area of ??constricted fibers, especially the surface of the ring structure. Afterwards, the authors confirmed the "ring-like" structure of migrasome, which was previously found by comparing confocal microscopy imaging with electron microscopic projection results.
After a series of drug treatments, the authors found that the formation of migrasome relies on cell migration and relies on the mobilization of cytoskeleton actin. In addition, in vitro overexpression experiments and animal tissue tests show that migrasome is widespread in various cell lines as well as in primary cells.
Finally, the authors found that during cell migration, the soma continually transported intracellular material to the migrasome. When cells release migrasome, these vesicles are engulfed by surrounding cells.
In summary, the authors demonstrate a new class of subcellular structures they found, "migrating bodies," through a series of biochemical means. Although its role in cell migration is unknown, the process clearly affects the intercellular communication. This finding complements the classic cell biology.
Recently, the International Journal of Cell Death & differentiation published a new study from MG Kolonin's group at the University of Texas Health Science Center in Houston using selective hunter-killer peptides to induce apoptosis of white adipose precursor cells The results showed that white adipose growth was inhibited in the model of hyperlipidemia-induced obesity and at the same time compensatory increase of beige adipocytes in adipose tissue was found. This may help us to target white adipose precursor cells, regulate white fat metabolism, Treatment of obesity provides a strategy.