+AAV在肝臟研究中的靶向策略【應(yīng)用篇】
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+案例分享 ‖ AAV9感染腸道組織
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肝臟方面:
1.
Proc. Natl. Acad. Sci. U.S.A. (PNAS). (IF=9.412). Zhang, et.al. (2020). Hepatic neddylation targets and stabilizes electron transfer flavoproteins to facilitate fatty acid β-oxidation.[中國(guó)人民解放軍軍事醫(yī)學(xué)科學(xué)院 & 南開(kāi)大學(xué) AAV-DJ-CAG-Cre II型戊二酸尿癥GA-II]
2.
Journal of Hepatology. (IF=20.582). She, et.al. (2019). PSMP/MSMP promotes hepatic ?brosis through CCR2 and represents a novel therapeutic target.[北京大學(xué)基礎(chǔ)醫(yī)學(xué)院 AAV8-hPSMP & null 肝纖維化]
3.
Theranostics. (IF=8.579). Liu, et.al. (2019). Suppression of YAP/TAZ-Notch1-NICD axis by bromodomain and extraterminal protein inhibition impairs liver regeneration.[浙江大學(xué) AAV9-CMV-YAP 肝再生]
4.
Molecular Cell. (IF=15.584). Wan, et.al. (2019). Pacer is a mediator of mTORC1 and GSK3-TIP60 signaling in regulation of autophagosome maturation and lipid metabolism.[浙江大學(xué) AAV9-mCherry-GFP-LC3 and AAV9-Pacerwt-HA&Pacer2KR-HA&PacerS157A-HA&PacerS157D-HA 肝自噬和脂代謝]
5.
Experimental Cell Research. (IF=3.383). Li, et.al. (2018). Brg1 promotes liver fibrosis via activation of hepatic stellate cells.[華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬同濟(jì)醫(yī)院 AAV8-shBrg1 or AAV8-GFP 肝纖維化]
6.
Molecular Cell. (IF=15.584). Wan, et.al. (2018). mTORC1-Regulated and HUWE1-Mediated WIPI2 Degradation Controls Autophagy Flux.[浙江大學(xué) AAV9-shHUWE1 & shNC and AAV9-WIPI2&WIPI2-S395A&WIPI2-S395D 肝自噬]
7.
Molecular Cell. (IF=15.584). Su, et.al. (2017). VPS34 Acetylation Controls Its Lipid Kinase Activity and the Initiation of Canonical and Non-canonical Autophagy.[浙江大學(xué) AAV9-CMV-VPS34&3KR&3KQ 肝自噬]
8.
Proc. Natl. Acad. Sci. U.S.A. (PNAS). (IF=9.412). He, et.al. (2017). MicroRNA-351 promotes schistosomiasis-induced hepatic fibrosis by targeting the vitamin D receptor.[第二軍醫(yī)大學(xué) AAV8-CMV-eGFP-miR-351-5p Sponge 血吸蟲(chóng)病肝纖維化]
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