日本和美國科學(xué)家組成的一個聯(lián)合研究小組日前在利用老鼠進(jìn)行的試驗(yàn)中,，成功發(fā)現(xiàn)視神經(jīng)再生機(jī)制,，同時使老鼠受損的視神經(jīng)實(shí)現(xiàn)了再生,。
東京都神經(jīng)科學(xué)綜合研究所研究員行方和彥,、原田高幸與美國科學(xué)家共同發(fā)現(xiàn),，一種名為“Dock3”的蛋白質(zhì)在視神經(jīng)細(xì)胞中發(fā)揮著重要作用,。向老鼠的視神經(jīng)細(xì)胞中植入能夠制造這種蛋白質(zhì)的基因后,，視神經(jīng)細(xì)胞活躍程度就會提高。
接下來,，科學(xué)家們利用一種轉(zhuǎn)基因老鼠與正常老鼠進(jìn)行對比試驗(yàn),。轉(zhuǎn)基因老鼠體內(nèi)制造“Dock3”蛋白質(zhì)的能力是正常老鼠的5倍左右。當(dāng)這兩種老鼠的視神經(jīng)受損后,，正常老鼠的視神經(jīng)幾乎不會再生,，但是轉(zhuǎn)基因老鼠的視神經(jīng)卻在很大程度上恢復(fù)了。
科學(xué)家由此認(rèn)為,，“Dock3”蛋白質(zhì)是使視神經(jīng)細(xì)胞活躍,，從而促進(jìn)視神經(jīng)再生的關(guān)鍵。由于人體內(nèi)也存在制造同樣蛋白質(zhì)的基因,，科學(xué)家期待這一研究成果能夠幫助開發(fā)出新的治療和預(yù)防視神經(jīng)受損的方法,。這一研究成果已經(jīng)刊登在新一期美國《國家科學(xué)院院刊》（PNAS）上。（生物谷Bioon.com）
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.0914514107
Dock3 induces axonal outgrowth by stimulating membrane recruitment of the WAVE complex
Kazuhiko Namekata a, Chikako Harada a,b, Choji Tayac, Xiaoli Guo a, Hideo Kimurad, Luis F. Paradab, and Takayuki Haradaa,b,1
Atypical Rho-guanine nucleotide exchange factors (Rho-GEFs) that contain Dock homology regions (DHR-1 and DHR-2) are expressed in a variety of tissues; however, their functions and mechanisms of action remain unclear. We identify key conserved amino acids in the DHR-2 domain that are critical for the catalytic activity of Dock-GEFs (Dock1–4). We further demonstrate that Dock-GEFs directly associate with WASP family verprolin-homologous (WAVE) proteins through the DHR-1 domain. Brain-derived neurotrophic factor (BDNF)-TrkB signaling recruits the Dock3/WAVE1 complex to the plasma membrane, whereupon Dock3 activates Rac and dissociates from the WAVE complex in a phosphorylation-dependent manner. BDNF induces axonal sprouting through Dock-dependent Rac activation, and adult transgenic mice overexpressing Dock3 exhibit enhanced optic nerve regeneration after injury without affecting WAVE expression levels. Our results highlight a unique mechanism through which Dock-GEFs achieve spatial and temporal restriction of WAVE signaling, and identify Dock-GEF activity as a potential therapeutic target for axonal regeneration.
