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EIKEN

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【公司名稱(chēng)】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
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細(xì)胞中蛋白折疊多數(shù)發(fā)生在內(nèi)質(zhì)網(wǎng)(ER)，但是如果這個(gè)過(guò)程出現(xiàn)差錯(cuò)，未折疊蛋白累積，對(duì)ER產(chǎn)生應(yīng)激。這可觸發(fā)UPR，關(guān)閉翻譯，降低未折疊蛋白，增加蛋白質(zhì)折疊機(jī)制的產(chǎn)生。然而，如果ER應(yīng)激沒(méi)有解決，UPR也能誘導(dǎo)凋亡。
兩個(gè)主要因素控制UPR-IRE1a和PERK。IRE1a通過(guò)激活轉(zhuǎn)錄因子X(jué)BP1促進(jìn)細(xì)胞存活，驅(qū)動(dòng)細(xì)胞存活基因的表達(dá)。另一方面，PERK激活一種轉(zhuǎn)錄因子稱(chēng)為CHOP，它反過(guò)來(lái)驅(qū)動(dòng)促凋亡因子DR5的表達(dá)。
舊金山加州大學(xué)Peter Walter及其同事現(xiàn)已證實(shí)CHOP激活DR5，表明它是一種細(xì)胞自主過(guò)程。但是他們也發(fā)現(xiàn)IRE1a抑制DR5，直接降解它的mRNA通過(guò)一種稱(chēng)為調(diào)節(jié)IRE1a依賴(lài)的降解(RIDD)過(guò)程。人類(lèi)癌細(xì)胞系出于ER應(yīng)激中的IRE1a抑制即可以防護(hù)DR5 mRNA降解又可以增加細(xì)胞凋亡。
每種生物都有一個(gè)共同的目標(biāo)：生存。它的所有體細(xì)胞都在協(xié)同工作，以保持它活著。它們是通過(guò)微調(diào)的溝通手段而達(dá)成目的的。聯(lián)合柏林和劍橋大學(xué)，盧森堡大學(xué)的盧森堡系統(tǒng)生物醫(yī)學(xué)中心(LCSB)的科學(xué)家*揭示細(xì)胞信號(hào)從周?chē)h(huán)境轉(zhuǎn)換為內(nèi)部信號(hào)的規(guī)律。就像一支管弦樂(lè)隊(duì)的一個(gè)孤立的音符，細(xì)胞的一個(gè)孤立信號(hào)處于次要性的地位。
“重要的是，該信號(hào)從細(xì)胞膜傳遞到細(xì)胞的強(qiáng)度和頻率的相對(duì)變化，”這項(xiàng)研究的*、LCSB的Alexander Skupin博士說(shuō)，這項(xiàng)研究發(fā)表于《science Signaling》雜志上。
通過(guò)使空氣振動(dòng)，一支管弦樂(lè)隊(duì)的樂(lè)器從而產(chǎn)生信號(hào)——音符。在細(xì)胞內(nèi)，鈣離子負(fù)責(zé)攜帶信號(hào)。當(dāng)來(lái)自于環(huán)境的一片信息——比如一個(gè)生物信使——與細(xì)胞的外膜相遇，細(xì)胞內(nèi)的鈣離子被釋放。在那里，鈣離子控制各種適應(yīng)過(guò)程。“乍一看，并沒(méi)有簡(jiǎn)單的離子沖動(dòng)模式，” Skupin解釋;“但它們?cè)诩?xì)胞內(nèi)仍然以一種有意義的反應(yīng)達(dá)到高潮，就像一個(gè)特定基因的激活。”
為了確定這一現(xiàn)象的潛在規(guī)律，研究人員結(jié)合成像技術(shù)和數(shù)學(xué)方法，研究人類(lèi)腎細(xì)胞和大鼠肝細(xì)胞。他們發(fā)現(xiàn)，鈣沖動(dòng)的強(qiáng)度和頻率經(jīng)歷了的變化——都發(fā)生在細(xì)胞-內(nèi)部和細(xì)胞-細(xì)胞之間。因此，它們所傳達(dá)的信息不能被孤立的信號(hào)單獨(dú)分析進(jìn)行解釋。“這就像在一個(gè)樂(lè)團(tuán)，在那里自己學(xué)習(xí)孤立的音符不容許有任何旋律的結(jié)果，”Skupin延續(xù)了音樂(lè)的比喻。 “你必須聽(tīng)聽(tīng)所有儀器的頻率和音量如何變化，以及產(chǎn)生旋律。然后你獲得了音樂(lè)作品的印象。”

現(xiàn)在，研究人員*成功地通過(guò)傾聽(tīng)細(xì)胞的交流而獲得這樣一整個(gè)印象。他們發(fā)現(xiàn)，鈣沖動(dòng)的過(guò)多變化導(dǎo)致彼此相對(duì)于一個(gè)特定的關(guān)系中：外部的刺激不會(huì)導(dǎo)致鈣沖動(dòng)的增長(zhǎng)，恰恰相反的是它們發(fā)生時(shí)的頻率有了變化——音樂(lè)廳中，交響曲中的儀器的音符會(huì)上升和下降。“這種模式是導(dǎo)致細(xì)胞反應(yīng)的實(shí)際信號(hào)，” Skupin說(shuō)。“我們的分析已經(jīng)對(duì)此提供了解釋。”
“這些結(jié)果對(duì)于分析疾病很重要，” LCSB的主任魯?shù)?middot;巴林教授說(shuō)。“我們知道，在帕金森病中，神經(jīng)細(xì)胞中的鈣平衡被破壞，并懷疑細(xì)胞之間的錯(cuò)誤通信可能在神經(jīng)退行性疾病的發(fā)病中發(fā)揮作用。隨著這些通信的基本規(guī)律的發(fā)現(xiàn)，如Alexander Skupin，他的團(tuán)隊(duì)和我們的合作伙伴現(xiàn)在已經(jīng)實(shí)現(xiàn)了，我們?cè)谂两鹕〉姆治鲋羞~進(jìn)了重要的一步。”
加州大學(xué)圣地亞哥分校醫(yī)學(xué)院的研究人員說(shuō)，調(diào)節(jié)細(xì)胞周期進(jìn)程(細(xì)胞分裂和復(fù)制的過(guò)程)中*的一種蛋白質(zhì)，實(shí)際上激活一個(gè)關(guān)鍵的抑癌基因，而不是像以前認(rèn)為的那樣使它失活。
“這項(xiàng)發(fā)現(xiàn)是我的實(shí)驗(yàn)室20年來(lái)的研究結(jié)果，” 加州大學(xué)圣地亞哥分校醫(yī)學(xué)院細(xì)胞和分子系的教授史蒂文·f·道迪博士說(shuō)。“它*抗原抗體了一個(gè)傳統(tǒng)的認(rèn)知，即一個(gè)稱(chēng)為p16-細(xì)胞周期蛋白D通路(癌癥中zui常見(jiàn)的遺傳通路突變)促進(jìn)所有腫瘤細(xì)胞的細(xì)胞周期進(jìn)程的一個(gè)基本方面。”這項(xiàng)研究結(jié)果發(fā)表于《eLife》雜志上。
細(xì)胞周期蛋白D是在細(xì)胞復(fù)制的*階段期間合成的，被認(rèn)為有助于促進(jìn)復(fù)雜的，多階段的過(guò)程，其中包括與視網(wǎng)膜母細(xì)胞瘤(Rb)蛋白的相互作用，Rb蛋白的功能是通過(guò)抑制細(xì)胞周期進(jìn)程防止細(xì)胞過(guò)度生長(zhǎng)，直到細(xì)胞準(zhǔn)備分裂。RB是一個(gè)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.