布魯氏菌IgG免疫熒光試劑盒

Brucella IgG IFA Kit

廣州健侖生物科技有限公司

主要用途：用于檢測狗血清中的布魯氏菌IgG抗體

產(chǎn)品規(guī)格：12 孔/張,10 張/盒

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布魯氏菌IgG免疫熒光試劑盒

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【公司名稱】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
【騰訊 】 2042552662
【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101-3室
【企業(yè)文化】

zui近劍橋大學的Evgeny Zatulovskiy 和 Rob Kay揭示網(wǎng)柱菌屬細胞，是研究細胞移動的通俗模式生物，能夠同時利用這兩種動力，提升它們也許相互干擾的問題。
為了解決這一問題，沃威克大學的Richard Tyson 和Till Bretschneider 開發(fā)了一項新計算機算法能夠追蹤大量的兩種泡和網(wǎng)柱菌屬細胞的顯微鏡電影中的偽突起。在目前的研究中，泡和偽突起在趨化作用期間如何合作，他們證明細胞形狀的影響怎樣影響這些動力相互作用。當緩慢的偽突起延伸它們的變形細胞膜創(chuàng)造一種內部彎曲區(qū)域。
在健康細胞中，TRAP-1是代謝的重要調節(jié)蛋白，并且已顯示出在調節(jié)線粒體能量生產(chǎn)中發(fā)揮的重要作用。在腫瘤細胞的線粒體中，TRAP-1是過量的。
Wistar研究所科學家創(chuàng)造了TRAP-1基因敲除小鼠，利用其來進行藥物Gamitrinib(其可靶定腫瘤細胞線粒體中的蛋白質)的研究。TRAP-1是熱休克90(HSP90)蛋白家族的一成員，腫瘤利用HSP90蛋白如TRAP-1，以幫助在治療下生存。
在腫瘤中，TRAP-1的缺失是有重大后果的，會觸發(fā)包括代謝問題的災難性缺陷，zui終導致腫瘤細胞死亡。然而，一開始就缺少TRAP-1的小鼠在子宮內有三周時間來補償此蛋白質的缺失。
研究人員發(fā)現(xiàn)，在他們的基因敲除小鼠中，TRAP-1的缺失會導致線粒體蛋白錯誤折疊，然后觸發(fā)代償性反應，導致細胞消耗更多的氧氣和代謝更多的糖。這將導致基因敲除小鼠線粒體產(chǎn)生失調水平的ATP。
線粒體活性的增加實際上會適度刺激氧化應激(自由基損傷)和相關的DNA損傷。雖然DNA損傷似乎不利于長壽養(yǎng)生，但低程度DNA損傷實際上減少了細胞的增殖，減慢生長速度，使細胞的自然修復機制生效。

Recently, Evgeny Zatulovskiy and Rob Kay of Cambridge University revealed that the cells of the genus Mycena, a popular model organism for studying the movement of cells, could exploit both of these motivations to enhance their mutual interference.
To tackle this problem, Richard Tyson and Till Bretschneider of Warwick University have developed a new computer algorithm that can track artifacts in a large number of microscopic films of both Bubble and Mycena cells. In the present study, how bubbles and pseudopromas work together during chemotaxis demonstrate how the effects of cell shape affect these kinetic interactions. When slow pseudoprojections extend their deformable cell membranes creating an inner curved area.
In healthy cells, TRAP-1 is an important regulatory protein of metabolism and has been shown to play an important role in the regulation of mitochondrial energy production. TRAP-1 is excessive in tumor cell mitochondria.
Wistar Institute scientists have created TRAP-1 knockout mice that allow them to study the drug Gamitrinib, which targets proteins in tumor cell mitochondria. TRAP-1 is a member of the heat shock 90 (HSP90) protein family that utilizes HSP90 proteins such as TRAP-1 to help survive the treatment.
In tumors, the absence of TRAP-1 has major consequences, triggering catastrophic defects that include metabolic problems that eventually lead to the death of tumor cells. However, mice lacking TRAP-1 initially had three weeks in the uterus to compensate for the protein loss.
The researchers found that in their knockout mice, the absence of TRAP-1 causes misfolding of mitochondrial proteins and triggers compensatory reactions that cause cells to consume more oxygen and metabolize more sugar. This will result in knockout of mitochondrial ATP levels in mice.
Increased mitochondrial activity can actually moderay stimulate oxidative stress (free radical damage) and related DNA damage. Although DNA damage seems to be detrimental to longevity, low levels of DNA damage actually reduce cell proliferation, slow the rate of growth and allow the cell's natural repair mechanism to work.