美國(guó)羅徹斯特大學(xué)神經(jīng)科學(xué)研究所發(fā)現(xiàn)了一種新蛋白,，并將它命名為“缺氧引導(dǎo)的線粒體運(yùn)動(dòng)調(diào)節(jié)器”（HUMMR）,。該蛋白的發(fā)現(xiàn)與對(duì)其功能的鑒定,，為人們研究線粒體的運(yùn)動(dòng)以及了解腦細(xì)胞如何應(yīng)對(duì)缺氧（如腦中風(fēng)而造成的傷害）,，提供了非常重要的基礎(chǔ),。相關(guān)研究報(bào)告發(fā)布在近期出版的《細(xì)胞生物學(xué)》雜志上,。
線粒體是細(xì)胞中非常重要的細(xì)胞器,，它們給細(xì)胞提供能量,，支持細(xì)胞活動(dòng),，并且可能還有助于細(xì)胞戰(zhàn)勝危害和損傷,。線粒體在細(xì)胞中必須合理地分布以便行使它們的功能。但是有一些特殊的細(xì)胞,，如大腦里的神經(jīng)元細(xì)胞,，具有非常特殊的形狀——有很多長(zhǎng)而突出的樹突和軸突，它們需要更加完善的調(diào)節(jié)機(jī)制來保證線粒體的正常分布,，以支持正常的細(xì)胞功能,。
經(jīng)過4年的研究,，羅切斯特大學(xué)神經(jīng)科學(xué)研究所的李艷博士和同事發(fā)現(xiàn)了HUMMR蛋白,，它能調(diào)節(jié)神經(jīng)元中線粒體的運(yùn)動(dòng)和分布。研究人員表示,，該蛋白的主要功能是保證細(xì)胞內(nèi)線粒體的正確分布,。如果細(xì)胞缺失這種蛋白，那么神經(jīng)元中大量的線粒體就離開它們正常的位置而回到胞體周圍,，只留下一些空洞的,、沒有線粒體支持的樹突和軸突。
當(dāng)大腦處在缺氧狀態(tài)下時(shí),，線粒體的功能受到限制,，無法給細(xì)胞提供足夠的能量。當(dāng)損傷達(dá)到一定程度，腦細(xì)胞就會(huì)不可避免地死亡,。理解線粒體運(yùn)動(dòng)的調(diào)節(jié)機(jī)制能幫助科學(xué)家們發(fā)現(xiàn)大腦是如何應(yīng)對(duì)和修復(fù)損傷的,。研究人員發(fā)現(xiàn)，HUMMR蛋白在缺氧的條件下出現(xiàn)高量表達(dá),。例如說,，腦中風(fēng)患者大腦有一段時(shí)間處于缺氧的狀態(tài)，這時(shí)該蛋白高量表達(dá)具有很重要的意義,。它可能會(huì)保證在這種病理狀態(tài)下線粒體在細(xì)胞中占領(lǐng)正確的位置,，以應(yīng)對(duì)病理損傷。研究人員認(rèn)為,，對(duì)于HUMMR蛋白和其他相關(guān)蛋白分子的研究對(duì)于預(yù)防和治療神經(jīng)疾病有很重要的意義,。（生物谷Bioon.com）
生物谷推薦原文出處：
JCB doi: 10.1083/jcb.200811033
HUMMR, a hypoxia- and HIF-1α–inducible protein, alters mitochondrial distribution and transport
Yan Li1,3, Seung Lim5, David Hoffman4, Pontus Aspenstrom6, Howard J. Federoff5, and David A. Rempe1,2,3
1Department of Neurology, Center for Neural Development and Disease, 2Interdepartmental Graduate Program in Neuroscience, 3Interdepartmental Graduate Program in Biomedical Genetics, and 4Department of Anesthesiology, University of Rochester School of Medicine & Dentistry, Rochester, NY 14642
5Georgetown University Medical Center, Washington, DC 20057
6Department of Microbiology, Tumour and Cell Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden
Mitochondrial transport is critical for maintenance of normal neuronal function. Here, we identify a novel mitochondria protein, hypoxia up-regulated mitochondrial movement regulator (HUMMR), which is expressed in neurons and is markedly induced by hypoxia-inducible factor 1 α (HIF-1α). Interestingly, HUMMR interacts with Miro-1 and Miro-2, mitochondrial proteins that are critical for mediating mitochondrial transport. Interestingly, knockdown of HUMMR or HIF-1 function in neurons exposed to hypoxia markedly reduces mitochondrial content in axons. Because mitochondrial transport and distribution are inextricably linked, the impact of reduced HUMMR function on the direction of mitochondrial transport was also explored. Loss of HUMMR function in hypoxia diminished the percentage of motile mitochondria moving in the anterograde direction and enhanced the percentage moving in the retrograde direction. Thus, HUMMR, a novel mitochondrial protein induced by HIF-1 and hypoxia, biases mitochondria transport in the anterograde direction. These findings have broad implications for maintenance of neuronal viability and function during physiological and pathological states.
