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中科院青促会会员

魏艳  博士 副研究员  

中国科学院青年创新促进会会员
中科院生物物理所,脑与认知科学国家重点实验室

研究方向:蛋白质异常修饰与代谢性疾病

电子邮件:yanwei@ibp.ac.cn

电       话:010-64888531

通讯地址:北京市朝阳区大屯路15号(100101)

英文版个人网页:http://english.ibp.cas.cn/faculty/index_18316.html?json=http://www.ibp.cas.cn/sourcedb_ibp_cas/cn/ibpexport/EN_zkyqchhy/202005/t20200519_5582909.json

 

简       历:

  2000.09 - 2005.06  北京大学护理学院,医学学士

  2005.09 - 2010.06  中国科学院生物物理研究所,理学博士

  2010.07 - 2014.12  中国科学院生物物理研究所,助理研究员

  2014.07 - 2014.10  澳大利亚昆士兰大学脑研究所,访问学者

  2015.08 - 2016.08  澳大利亚昆士兰大学脑研究所,国家公派访问学者

  2015.01 - 至今       中国科学院生物物理研究所,副研究员

获奖及荣誉:

 

社会任职:

 

研究方向:

  从分子、细胞、动物水平研究蛋白质异常修饰(磷酸化、糖基化等)的促发因素、错误折叠以及与代谢性疾病的关系。

承担项目情况:

  1. 国家自然科学基金面上项目《核糖代谢异常在糖尿病脑病中的作用及机制研究》,2017-2020,直接经费60万,负责人

  2. 国家青年科学基金项目《核糖糖基化导致Tau蛋白超磷酸化的分子机制研究》,2013-2015,23万,负责人

代表论著:

  1. Yu LX, Chen Y, Xu Y, He T, Wei Y#, He RQ#. D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy. Aging (Albany NY), 2019, 11(14):4943-4969. (#co-corresponding authors)

  2. Wu BB, Wang YJ, Shi CG, Chen Y, Yu LX, Li J, Li WW, Wei Y#, He RQ#. Ribosylation-Derived Advanced Glycation End Products Induce Tau Hyperphosphorylation Through Brain-Derived Neurotrophic Factor Reduction. J Alzheimers Dis, 2019, 71(1):291-305.

  3. Wu BB, Yu LX, Hu PD, Lu Y, Li J, Wei Y#, He RQ#. GRP78 protects CHO cells from ribosylation. BBA-Mol Cell Res, 2018, 1865:629-637. (#co-corresponding authors)

  4. Chen XX, Su T, Chen Y, He YG, Liu Y, Xu Y, Wei Y#, Li J, He RQ#. D-Ribose as a Contributor to Glycated Haemoglobin. Ebiomedicine, 2017, 25:143-153. (#co-corresponding authors)

  5. Hatch RJ, Wei Y, Xia D, Goetz J. Hyperphosphorylated tau causes reduced hippocampal CA1 excitability by relocating the axon initial segment. Acta Neuropathol, 2017, 133(5):717-730.

  6. Li T, Su T, He YG, Lu JH, Mo WC, Wei Y#, He RQ#. Brain formaldehyde is related to water intake behavior. Aging Dis, 2016, 10.14336/AD.2016.0323. ( #co-corresponding authors)

  7. Wei Y*, Wang YJ*, Wu BB, Zhang YH, He RQ. Ribosylated BSA monomer is severely toxic to SH-SY5Y cells. Prog Biochem Biophys, 2016, 43(6):579-591. (* co-first authors)

  8. Wu BB*, Wei Y*, Wang YJ, Su T, Zhou L, Liu Y, He RQ. Gavage of D-Ribose induces Aβ-like deposits, Tau hyperphosphorylation as well as memory loss and anxiety-like behavior in mice. Oncotarget, 2015, 6(33):34128-42. (* co-first authors)

  9. Wei Y, Han CS, Wang YJ, Wu BB, Su T, Liu Y, He RQ. Ribosylation triggering Alzheimer’s disease-like Tau hyperphosphorylation via activation of CaMKII. Aging Cell, 2015, 14(5):754-763.

  10. Han CS, Lu Y, Wei Y#, Wu BB, Liu Y, He RQ#. D-Ribosylation induces cognitive impairment through RAGE-dependent astrocytic inflammation. Cell Death Dis, 2014, 5, e1117. ( #co-corresponding authors)

  11. Lu Y, He HJ, Zhou J, Miao JY, Lu J, He YG, Pan R, Wei Y#, Liu Y, He RQ#. Hyperphosphorylation results in tau dysfunction in DNA folding and protection. J Alzheimers Dis, 2013, 37:551-563. ( #co-corresponding authors)

  12. Wei Y, Han CS, Zhou J, Liu Y, Chen L, He RQ. D-ribose in glycation and protein aggregation. Biochim Biophys Acta, 2012, 1820(4):488-494.

  13. Liu YY, Qiang M, Wei Y, He RQ. A novel molecular mechanism for nitrated alpha-synuclein-induced cell death. J Mol Cell Biol, 2011, 3:239–249.

  14. Chen L*, Wei Y*, Wang XQ, He RQ. Ribosylation rapidly induces a-synuclein to form highly cytotoxic molten globules of advanced glycation end products. PLoS ONE, 2010, 5(2):e9052. (* co-first authors)

  15. Wei Y*, Chen L*, Chen J, Ge L, He RQ. Rapid glycation with D-ribose induces globular amyloid-like aggregations of BSA with high cytotoxicity to SH-SY5Y cells. BMC Cell Biol, 2009, 10:10. (* co-first authors)

  16. Wei Y*, Qu MH*, Wang SX, Chen L, Wang DL, Liu Y, Hua Q, He RQ. Binding to the Minor Groove of the Double-Strand, Tau Protein Prevents DNA from Damage by Peroxidation. PLoS ONE, 2008, 3(7): e2600. (* co-first authors)

 

(资料来源:魏艳副研究员,2020-10-27)