+應(yīng)用篇|AAV在肌肉組織中的靶向策略
+干貨篇|AAV在肌肉組織中的靶向應(yīng)用策略
+『AAV-骨骼系統(tǒng)』如何實(shí)現(xiàn)外源基因在骨骼系統(tǒng)的高效表達(dá)?
+AAV在內(nèi)耳的靶向應(yīng)用策略(下)
+『重磅盤(pán)點(diǎn)』AAV在腎臟研究中的應(yīng)用策略
+『應(yīng)用篇』AAV在腎臟研究中的案例分享
+『干貨篇』AAV在肺部應(yīng)用中的靶向策略
+『應(yīng)用篇』AAV在肺部應(yīng)用中的靶向策略
+維真腺相關(guān)病毒在腎病研究中的應(yīng)用
+IF=8.702|北京協(xié)和醫(yī)院研究團(tuán)隊(duì)發(fā)現(xiàn)血-睪屏障調(diào)控新機(jī)制!
皮膚方面:
1.
International Journal of Biological Sciences. (IF=4.858). Wu, et.al. (2019). Metformin Promotes the Survival of Random-Pattern Skin Flaps by Inducing Autophagy via the AMPK-mTOR-TFEB signaling pathway.[溫州醫(yī)科大學(xué)附屬第二醫(yī)院 AAV9-U6-shRNA (Prkaa1)-CMV-EGFP 隨意皮瓣]
腎臟方面:
EBIOMEDICINE. (IF=5.736). Liu, et.al. (2019). H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway.[華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬同濟(jì)醫(yī)院 AAV9-H19 腎鈣質(zhì)沉著癥]
2.
Science Translational Medicine. (IF=16.304). Wang, et.al. (2018). Long noncoding RNA lnc-TSI inhibits renal fibrogenesis by negatively regulating the TGF-β/Smad3 pathway.[南方醫(yī)科大學(xué) AAV9-MIR-GFP-lnc-TSI 腎纖維化]
肺臟方面:
Cell Death & Disease. (IF=6.304). Zhang, et.al. (2019). circHIPK3 regulates lung fibroblast-to-myofibroblast transition by functioning as a competing endogenous RNA.[上海市第一人民醫(yī)院 AAV6-circHIPK3 shRNA & scrambled shRNA 肺纖維化]
Oncotarget. Tian, et.al. (2017). Sirtuin 6 inhibits epithelial to mesenchymal transition during idiopathic pulmonary fibrosis via inactivating TGF-β1/Smad3 signaling.[華中科技大學(xué)同濟(jì)醫(yī)學(xué)院公共衛(wèi)生學(xué)院 AAV-Sirt6 特發(fā)性肺纖維化]
體外實(shí)驗(yàn):
Retrovirology. (IF=4.183). Wang, et.al. (2017). Genome modifcation of CXCR4 by Staphylococcus aureus Cas9 renders cells resistance to HIV-1 infection.[武漢大學(xué)基礎(chǔ)醫(yī)學(xué)院 AAV-SaCas9-CXCR4-gRNA HIV基因治療]
巨噬細(xì)胞方面:
EBioMedicine. (IF=5.736). Lian, et.al. (2019). Macrophage metabolic reprogramming aggravates aortic dissection through the HIF1α-ADAM17 pathway. [北京大學(xué) AAV2-ADAM17-GFP & AAV2-GFP 主動(dòng)脈夾層AD]
Circulation Research. (IF=14.467). Fu, et.al. (2016). Shift of Macrophage Phenotype Due to Cartilage Oligomeric Matrix Protein Defciency Drives Atherosclerotic Calcifcation. [北京大學(xué) AAV2-integrin β3 & AAV2-β-tail domain & AAV2-GFP 動(dòng)脈粥樣硬化AS]
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