落基山斑疹傷寒立克次體IgM ELISA試劑盒

落基山斑疹傷寒立克次體IgM ELISA試劑盒

Rickettsia rickettsii IgM ELISA Kit

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)人血清中的落基山斑疹傷寒立克次體IgM抗體

產(chǎn)品規(guī)格：96人份/盒

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落基山斑疹傷寒立克次體IgM ELISA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(hào)二期2幢101-3室
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形成一個(gè)功能性動(dòng)力蛋白-2馬達(dá)需要這兩個(gè)基因編碼的蛋白質(zhì)，這就解釋了為什么任一個(gè)基因發(fā)生突變都會(huì)引發(fā)ciliopathy。這項(xiàng)工作還確定了動(dòng)力蛋白-2的新組分(TCTEX1D2)，提供一個(gè)候選基因，其突變或可導(dǎo)致年輕綜合征。
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)。

The formation of a functional dynein-2 motor requires proteins encoded by both genes, which explains why mutations in either gene can trigger ciliopathy. This work also identified a new component of dynein-2 (TCTEX1D2), which provides a candidate gene whose mutation may lead to young syndrome.
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 in 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 .