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【公司名稱】 廣州健侖生物科技有限公司
【】    楊永漢 
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隨著越來越多的結(jié)構(gòu)變得可用，研究人員希望調(diào)整AWSEM膜算法。Wolynes說：“我不認(rèn)為我們已經(jīng)了解膜的相互作用。”這表明大部分的漏斗形折疊發(fā)生在蛋白質(zhì)進(jìn)入膜之后，很少是因為疏水性(動力學(xué))相互作用，疏水性相互作用在球狀蛋白質(zhì)折疊中發(fā)揮了更大的作用。他說：“我的直覺是，那將是正確的。”
Wolynes說：“本文的意義在于，現(xiàn)在我們有一種運(yùn)算法則，可根據(jù)原始的基因組序列，相當(dāng)好地預(yù)測膜蛋白結(jié)構(gòu)。這對于解釋新一代的實(shí)驗結(jié)果將非常的有用。”
從受精卵到成年人，人類細(xì)胞需要經(jīng)歷的分裂次數(shù)可以說是天文數(shù)字。每一次分裂時，母細(xì)胞都必須將DNA精確分配給兩個子細(xì)胞。而著絲粒的完整性是細(xì)胞成功分裂的關(guān)鍵。著絲粒是染色體上的一個特殊DNA區(qū)域，是紡錘絲微管的附著之處，也是姐妹染色單體在分開前相互連接的地方。分離染色體的微管要識別著絲粒，需要該區(qū)域富含一種關(guān)鍵的蛋白——CENP-A。在細(xì)胞進(jìn)行DNA復(fù)制準(zhǔn)備分裂的時候，需要確保新舊DNA鏈的著絲粒區(qū)域填充有足夠的CENP-A。在此之前人們只知道著絲粒在G1期填充CENP-A，但并不了解這一過程的具體調(diào)控機(jī)制。
在這項研究中，懷特海德研究所的McKinley發(fā)現(xiàn)了兩種確保CENP-A正確填充的關(guān)鍵激酶，Plk1和CDK。這兩種激酶參與了CENP-A填充的不同步驟，只有它們都正常起作用，CENP-A才能填滿著絲粒中的所有空隙。McKinley不僅解析了這些激酶的作用途徑，還在此基礎(chǔ)上干擾了CENP-A的填充時機(jī)，研究顯示這種干擾會引起嚴(yán)重的染色體分離問題。
“著絲粒的功能處于嚴(yán)格的控制之下，因此人們一直認(rèn)為CENP-A的填充時機(jī)應(yīng)該很重要?，F(xiàn)在，我們終于證實(shí)了這一理論，”McKinley說。
“CENP-A填充是著絲粒形成的核心步驟，”Cheeseman說，他也是MIT的生物學(xué)副教授。 “這項研究揭示了這一步驟的調(diào)控基礎(chǔ)，有助于我們深入理解細(xì)胞分裂的具體過程。”
干細(xì)胞可替代中樞神經(jīng)系統(tǒng)損傷后丟失的細(xì)胞，減少神經(jīng)組織損害，促進(jìn)功能恢復(fù)。許多腦損傷模型，如大腦中動脈阻塞和創(chuàng)傷性腦損傷模型中均證實(shí)神經(jīng)干細(xì)胞可從腦室下區(qū)遷移至大腦皮質(zhì)損傷區(qū)。但目前仍不夠清晰的問題是，激活缺血大腦內(nèi)源性神經(jīng)干細(xì)胞的機(jī)制何在?
韓國全南國立大學(xué)醫(yī)學(xué)院法醫(yī)學(xué)系Hyung-Seok Kim博士所在課題組的研究揭示，局灶性腦缺血后神經(jīng)干細(xì)胞的激活存在時序性，并驗證了早期表達(dá)的低氧誘導(dǎo)因子1α和血管內(nèi)皮生長因子組成的微環(huán)境提高了腦缺血后激活的內(nèi)源性神經(jīng)干細(xì)胞神經(jīng)可塑性。大腦皮質(zhì)損傷后，神經(jīng)前體細(xì)胞的損失可由損傷周圍區(qū)域和腦室下區(qū)得以補(bǔ)充。

As more and more structures become available, researchers hope to adapt the AWSEM membrane algorithm. Wolynes said: "I do not think we have understood the membrane interactions." This shows that most of the funnel-shaped folds occur after the proteins enter the membrane, seldom because of hydrophobic (kinetic) interactions, hydrophobic interactions in the globular Protein folding has played a greater role. He said: "My intuition is that it will be right."
Wolynes says: "What this article means is that now we have an algorithm that fairly predicts the membrane protein structure based on the original genome sequence, which is very useful to explain the new generation of experiments."
From fertilized eggs to adults, the number of divisions human cells need to go through can be said to be astronomical. Each division, the mother cell must be precisely allocated to two daughter cells. The integrity of the centromere is the key to successful cell division. Centromeres are a special DNA region on chromosomes, where spindle microtubules attach themselves and where sister chromatids are connected before they are separated. Microtubules that separate chromosomes recognize centromeres and require this region to be enriched with a key protein, CENP-A. When the cell is ready for DNA replication, it is necessary to ensure that the centromeric regions of the new and old DNA strands are filled with sufficient CENP-A. Before that, people only knew that centromere filled CENP-A in G1 phase, but did not understand the specific regulation mechanism of this process.
In this study, McKinley at the Whitehead Institute identified two key kinases, Plk1 and CDK, that ensure correct filling of CENP-A. These two kinases are involved in different steps of CENP-A packing, and only if they both function normally, CENP-A can fill all the voids in the centromere. Not only did McKinley interpret the pathway of action of these kinases, but they also interfered with the timing of filling CENP-A, and studies showed that this interference can cause serious chromosomal segregation problems.
"The centromere function is under tight control, so it has been argued that the timing of filling with CENP-A should be important, and we have finally confirmed that," McKinley said.
"CENP-A packing is a central step in centromere formation," said Cheeseman, who is also an associate professor of biology at MIT. "This study reveals the basis for the regulation and control of this step, helping us to understand the specific process of cell division."
Stem cells can replace lost cells after CNS injury, reduce nerve tissue damage and promote functional recovery. Many brain injury models, such as middle cerebral artery occlusion and traumatic brain injury models, have confirmed that neural stem cells can migrate from the subventricular zone to the cerebral cortical lesion. However, the question remains unclear: what is the mechanism of activation of endogenous neural stem cells in ischemic brain?
A study by Dr. Hyung-Seok Kim, MD, from the Department of Forensic Medicine, Jeonnam National University School of Medicine, Korea, revealed that the activation of neural stem cells after focal cerebral ischemia is time-sequential and validates the early expression of hypoxia-inducible factor-1α and vascular endothelial Microenvironment of growth factor enhances the neuroplasticity of endogenous neural stem cells activated after cerebral ischemia. After cortical injury, the loss of neural progenitor cells can be compensated for by the area surrounding the lesion and the subventricular zone.