肺炎链球菌检测试剂盒（免疫捕获法）

EIKEN肺炎链球菌检测试剂盒（免疫捕获法）

广州健仑生物科技有限公司

主要用途：用于检测尿标本中的肺炎链球菌抗原，以支持肺炎链球菌感染的诊断。

产品规格：20T/盒

存储条件：2-30℃

EIKEN肺炎链球菌检测试剂盒（免疫捕获法）

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【产品介绍】

EIKEN

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【公司名称】 广州健仑生物科技有限公司
【】    杨永汉 
【】 
【腾讯 】 2042552662
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-3室
【企业文化】

细胞中蛋白折叠多数发生在内质网(ER)，但是如果这个过程出现差错，未折叠蛋白累积，对ER产生应激。这可触发UPR，关闭翻译，降低未折叠蛋白，增加蛋白质折叠机制的产生。然而，如果ER应激没有解决，UPR也能诱导凋亡。
两个主要因素控制UPR-IRE1a和PERK。IRE1a通过激活转录因子XBP1促进细胞存活，驱动细胞存活基因的表达。另一方面，PERK激活一种转录因子称为CHOP，它反过来驱动促凋亡因子DR5的表达。
旧金山加州大学Peter Walter及其同事现已证实CHOP激活DR5，表明它是一种细胞自主过程。但是他们也发现IRE1a抑制DR5，直接降解它的mRNA通过一种称为调节IRE1a依赖的降解(RIDD)过程。人类癌细胞系出于ER应激中的IRE1a抑制即可以防护DR5 mRNA降解又可以增加细胞凋亡。
每种生物都有一个共同的目标：生存。它的所有体细胞都在协同工作，以保持它活着。它们是通过微调的沟通手段而达成目的的。联合柏林和剑桥大学，卢森堡大学的卢森堡系统生物医学中心(LCSB)的科学家*揭示细胞信号从周围环境转换为内部信号的规律。就像一支管弦乐队的一个孤立的音符，细胞的一个孤立信号处于次要性的地位。
“重要的是，该信号从细胞膜传递到细胞的强度和频率的相对变化，”这项研究的*、LCSB的Alexander Skupin博士说，这项研究发表于《science Signaling》杂志上。
通过使空气振动，一支管弦乐队的乐器从而产生信号——音符。在细胞内，钙离子负责携带信号。当来自于环境的一片信息——比如一个生物信使——与细胞的外膜相遇，细胞内的钙离子被释放。在那里，钙离子控制各种适应过程。“乍一看，并没有简单的离子冲动模式，” Skupin解释;“但它们在细胞内仍然以一种有意义的反应达到高潮，就像一个特定基因的激活。”
为了确定这一现象的潜在规律，研究人员结合成像技术和数学方法，研究人类肾细胞和大鼠肝细胞。他们发现，钙冲动的强度和频率经历了的变化——都发生在细胞-内部和细胞-细胞之间。因此，它们所传达的信息不能被孤立的信号单独分析进行解释。“这就像在一个乐团，在那里自己学习孤立的音符不容许有任何旋律的结果，”Skupin延续了音乐的比喻。 “你必须听听所有仪器的频率和音量如何变化，以及产生旋律。然后你获得了音乐作品的印象。”

现在，研究人员*成功地通过倾听细胞的交流而获得这样一整个印象。他们发现，钙冲动的过多变化导致彼此相对于一个特定的关系中：外部的刺激不会导致钙冲动的增长，恰恰相反的是它们发生时的频率有了变化——音乐厅中，交响曲中的仪器的音符会上升和下降。“这种模式是导致细胞反应的实际信号，” Skupin说。“我们的分析已经对此提供了解释。”
“这些结果对于分析疾病很重要，” LCSB的主任鲁迪·巴林教授说。“我们知道，在帕金森病中，神经细胞中的钙平衡被破坏，并怀疑细胞之间的错误通信可能在神经退行性疾病的发病中发挥作用。随着这些通信的基本规律的发现，如Alexander Skupin，他的团队和我们的合作伙伴现在已经实现了，我们在帕金森病的分析中迈进了重要的一步。”
加州大学圣地亚哥分校医学院的研究人员说，调节细胞周期进程(细胞分裂和复制的过程)中*的一种蛋白质，实际上激活一个关键的抑癌基因，而不是像以前认为的那样使它失活。
“这项发现是我的实验室20年来的研究结果，” 加州大学圣地亚哥分校医学院细胞和分子系的教授史蒂文·f·道迪博士说。“它*抗原抗体了一个传统的认知，即一个称为p16-细胞周期蛋白D通路(癌症中zui常见的遗传通路突变)促进所有肿瘤细胞的细胞周期进程的一个基本方面。”这项研究结果发表于《eLife》杂志上。
细胞周期蛋白D是在细胞复制的*阶段期间合成的，被认为有助于促进复杂的，多阶段的过程，其中包括与视网膜母细胞瘤(Rb)蛋白的相互作用，Rb蛋白的功能是通过抑制细胞周期进程防止细胞过度生长，直到细胞准备分裂。RB是一个抑癌基因。

The majority of protein folding in cells occurs in the endoplasmic reticulum (ER), but if there is a mistake in this process, unfolded protein accumulates, stressing the ER. This triggers UPR, turning off translation, reducing unfolded proteins, and increasing the production of protein folding mechanisms. However, UPR also induces apoptosis if ER stress is not resolved.
Two major factors control UPR-IRE1a and PERK. IRE1a promotes cell survival by activating the transcription factor XBP1, driving the expression of cell-survival genes. On the other hand, PERK activates a transcription factor called CHOP, which in turn drives the expression of pro-apoptotic factor DR5.
Peter Walter and colleagues at the University of California, San Francisco, have now shown that CHOP activates DR5, indicating that it is a cell-autonomous process. However, they also found that IRE1a inhibits DR5 by directly degrading its mRNA through a process called regulation of IRE1a-dependent degradation (RIDD). Human cancer cell lines protect DR5 mRNA from degradation and increase apoptosis as well, due to IRE1a inhibition in ER stress.
Each creature has a common goal: to survive. All its somatic cells are working together to keep it alive. They do this by fine-tuning the means of communication. For the first time, scientists at the Luxembourg Systemic Biomedicine Center (LCSB) in Berlin and the University of Cambridge, University of Luxembourg, have uncovered the law that cellular signals are converted from the surrounding environment to internal signals. Like an isolated note of an orchestra, an isolated signal of the cell is secondary.
"Importantly, the relative change in the intensity and frequency of the signal delivered from the cell membrane to the cell," said Alexander Skupin, MD, Ph.D., a study lead author of the study in the journal Science Signaling.
By vibrating the air, an orchestra's instrument produces a signal-note. Within the cell, calcium is responsible for carrying the signal. When a piece of information from the environment - such as a bio-messenger - meets the outer membrane of a cell, intracellular calcium is released. There, calcium ions control various adaptation processes. "At first glance, there is no simple model of ion impulses," Skupin explains; "but they still culminate in a meaningful reaction in the cell, much like the activation of a particular gene."
To determine the underlying law of this phenomenon, researchers used both imaging techniques and mathematical methods to study human kidney cells and rat hepatocytes. They found that the intensity and frequency of calcium impulses underwent extreme changes-both in the cell-interior and cell-cell. Therefore, the information they convey can not be interpreted individually by isolated signals. "It's like in an orchestra where studying isolated or isolated notes does not allow any melody to result," Skupin continues the metaphor of music. "You have to hear how the frequency and volume of all the instruments change, and the melodies." Then you get the impression of a piece of music. "

Now, for the first time, researchers have been able to get such an impression by listening to the exchange of cells. They found that too many changes in calcium impulses lead to one another relative to a particular relationship: external stimuli do not lead to an absolute increase in calcium impulses, but instead the frequency at which they occur has changed - in concert halls, symphonic The notes in the instrument will rise and fall. "This pattern is the actual signal that leads to cellular responses," Skupin said. "Our analysis has provided an explanation for this."
"These results are important for disease analysis," said Rudy Bahrain, director of LCSB. "We know that in Parkinson's disease the balance of calcium in nerve cells is broken and it is suspected that miscommunication between cells may play a role in the pathogenesis of neurodegenerative diseases.With the discovery of the basics of these communications, Alexander Skupin, his team and our partners have now come true and we are taking an important step in the analysis of Parkinson's disease. "
Researchers at the University of California San Diego School of Medicine say a protein essential for the process of regulating the cell cycle (the process of cell division and replication) actually activates a key tumor suppressor rather than, as previously thought, It is inactivated.
"This finding is the result of two decades of my laboratory's research," said Dr. Steven F. Dodi, a professor of cellular and molecular medicine at the University of California San Diego School of Medicine. "It's a compley traditional understanding of antigen-antibody, a fundamental aspect of what is known as the p16-cyclin D pathway, the most common genetic pathway mutation in cancer, that promotes the cell cycle progression of all tumor cells." The study Results published in the "eLife" magazine.
Cyclin D, which is synthesized during the first phase of cell replication, is thought to contribute to the promotion of a complex, multi-stage process including the interaction with retinoblastoma (Rb) proteins whose function is Prevent cell overgrowth by inhibiting cell cycle progression until the cell is ready for division. RB is a tumor suppressor gene.