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西班牙Certest嗜肺軍團(tuán)菌單抗(克隆LN29)

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西班牙Certest嗜肺軍團(tuán)菌單抗(克隆LN29)

日本理化學(xué)研究所(RIKEN)腦科學(xué)研究所的研究人員，聯(lián)合順天堂大學(xué)和日本科學(xué)技術(shù)振興機(jī)構(gòu)，發(fā)現(xiàn)一種廣泛參與細(xì)胞內(nèi)鈣信號(hào)轉(zhuǎn)導(dǎo)的細(xì)胞受體——IP3受體——可通過酶的作用被鎖定在閉合狀態(tài)中，且該鎖定作用可能在神經(jīng)變性中出現(xiàn)的神經(jīng)信號(hào)減少中發(fā)揮作用，如亨廷頓氏和阿爾茨海默氏病。
在發(fā)表于當(dāng)前的《PNAS》雜志上的研究中，科學(xué)家報(bào)道了，在人類細(xì)胞和亨廷頓氏病的小鼠模型的實(shí)驗(yàn)中，揭示2型轉(zhuǎn)谷氨酰胺酶——一種在神經(jīng)變性疾病患者中的細(xì)胞升高的蛋白交聯(lián)酶——與IP3受體相互作用，將其鎖定在在一個(gè)封閉的非功能性結(jié)構(gòu)中，阻止其履行必要的鈣釋放作用。他們確定了該受體上的一個(gè)特定的氨基酸位點(diǎn)，Gln2746，其可以進(jìn)行修飾作用，這項(xiàng)研究加深了我們對(duì)于受體如何被鎖定的理解，以及可能打開了通過構(gòu)象變化來(lái)研究其他功能蛋白的大門。
IP3受體通道位于內(nèi)質(zhì)網(wǎng)上，在細(xì)胞內(nèi)鈣信號(hào)傳導(dǎo)中發(fā)揮至關(guān)重要作用，并參與多種細(xì)胞功能，包括線粒體能量產(chǎn)生和自噬調(diào)節(jié)。雖然自噬通常情況下是維持細(xì)胞維修的一個(gè)機(jī)制，但它也可以觸發(fā)細(xì)胞功能的喪失，并明顯與一些神經(jīng)變性疾病有關(guān)，包括亨廷頓氏病，阿爾茨海默氏病和帕金森氏病有關(guān)。
在這項(xiàng)工作中，科學(xué)家提出了一個(gè)通用的模型發(fā)現(xiàn)，由2型轉(zhuǎn)谷氨酰胺酶的作用造成異常的IP3受體介導(dǎo)的鈣信號(hào)轉(zhuǎn)導(dǎo)，導(dǎo)致細(xì)胞功能紊亂，隨后出現(xiàn)大腦功能障礙。轉(zhuǎn)谷氨酰胺酶2的激活通常與炎癥和應(yīng)激有關(guān)，以及IP3通道上的轉(zhuǎn)谷氨酰胺酶2作用，可能會(huì)為常見于不同的神經(jīng)變性疾病的發(fā)生和發(fā)展步驟提供一個(gè)證據(jù)。
這項(xiàng)研究的*Katsuhiko Mikoshiba說(shuō)：“我們認(rèn)為，我們?cè)谶@項(xiàng)研究中所確定的機(jī)制，可以為我們提供一個(gè)研究大腦和身體的其他部位的其他疾病的通用模型，其中2型轉(zhuǎn)谷氨酰胺酶被上調(diào)。我們希望這種認(rèn)知zui終可能為許多神經(jīng)退行性疾病開發(fā)新的藥物療法，這些疾病為患者和社會(huì)帶來(lái)沉重的負(fù)擔(dān)。”
大約50年前，電子顯微鏡揭示了細(xì)胞內(nèi)形成的類似斑點(diǎn)的結(jié)構(gòu)，它們到處移動(dòng)然后消失。但科學(xué)家們并不知道它們存在的意義——據(jù)稱這些移動(dòng)的類似云的蛋白質(zhì)集合對(duì)細(xì)胞生命至關(guān)重要，因此它們或可能提供疾病治療的新方法。
在期刊《細(xì)胞生物學(xué)》上發(fā)表在一項(xiàng)研究里，兩名研究人員呼吁不同背景的科研者，從生物學(xué)到細(xì)胞生物學(xué)，將關(guān)注點(diǎn)集中在這些構(gòu)造的用途上，他們啟用了一個(gè)統(tǒng)一的術(shù)語(yǔ)“集合體”來(lái)指代它們。
“我想要了解尤文肉瘤里的這些集合體在做什么，尤文肉瘤是我正在關(guān)注研究的疾病，我認(rèn)為所有研究人體生物學(xué)的其他科研人員應(yīng)該也會(huì)想要知道集合體在健康人群和疾病人群里所發(fā)揮的功能。” 喬治敦倫巴狄綜合癌癥中心腫瘤學(xué)和兒科學(xué)學(xué)院的教授杰弗里·托雷茨基(Jeffrey Toretsky)這樣說(shuō)道。

西班牙Certest嗜肺軍團(tuán)菌單抗(克隆LN29)

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【公司名稱】 廣州健侖生物科技有限公司
【市場(chǎng)部】    楊永漢

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【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(hào)二期2幢101-103室

Researchers at the RIKEN Institute for Brain Science, in collaboration with Sun Yat-Sen University and Japan's Agency for the Advancement of Science and Technology, have found that a cellular receptor widely involved in intracellular calcium signaling, the IP3 receptor, The action of the enzyme is locked in a closed state and this locking effect may play a role in the reduction of neural signals that occur in neurodegeneration such as Huntington's and Alzheimer's disease.
In a study published in the current issue of PNAS, scientists reported that experiments in mouse models of human cells and Huntington's disease revealed that type 2 transglutaminase, a protein found in patients with neurodegenerative diseases The cell-augmented protein-linked enzyme, which interacts with the IP3 receptor, locks it in a closed, non-functional structure that prevents it from performing the necessary calcium release. They identified a specific amino acid site on the receptor, Gln2746, which can be modified, deepening our understanding of how receptors are locked and possibly opening up the possibility of studying other functional proteins through conformational changes The door.
The IP3 receptor channel, located on the endoplasmic reticulum, plays a crucial role in intracellular calcium signaling and is involved in a variety of cellular functions including mitochondrial energy production and autophagy regulation. Although autophagy is usually a mechanism for maintaining cell maintenance, it can also trigger the loss of cellular function and is clearly associated with several neurodegenerative diseases, including Huntington's disease, Alzheimer's disease and Parkinson's disease .
In this work, scientists propose a generic model that found that aberrant IP3 receptor-mediated calcium signaling caused by type 2 transglutaminase leads to cellular dysfunction followed by brain dysfunction. Activation of transglutaminase 2, which is usually associated with inflammation and stress, and transglutaminase 2 action on the IP3 channel, may provide evidence of the common occurrence and progression of various neurodegenerative diseases.
Katsuhiko Mikoshiba, leader of the study, said: "We think the mechanism we identified in this study can provide us with a generic model for studying other diseases of the brain and other parts of the body, of which type 2 transglutaminase Amidase is up-regulated, and we hope this perception could ultimay lead to the development of new drug regimens for many neurodegenerative diseases that put a heavy burden on patients and society. "
About 50 years ago, electron microscopy revealed similar spots in the cell structure, they move around and disappear. But scientists do not know the meaning of their existence - these moving cloud-like protein collections are said to be vital to cell life and therefore they may or may provide new ways of treating the disease.
In a study published in the journal Cell Biology, two researchers called for researchers of diverse backgrounds, from biology to cell biology, to focus on the uses of these constructs, enabling a unified The term "aggregate" refers to them.
"I want to know what these assemblies in Ewing's sarcoma are doing, and Ewing's sarcoma is a disease I'm focusing on, and I think all other researchers working on human biology should also want to know how the aggregates are found in healthy people and diseases People, "said Jeffrey Toretsky, a professor at the Oncology and Paediatrics School at the Georgetown Comprehensive Cancer Center in Georgetown.