Yan Wei, Ph.D, Associate Professor
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Member of the Youth Innovation Promotion Association of CAS
State Key Laboratory of Brain & Cognitive Sciences, IBP
Research Interests: Protein modification and metabolic disorders
Email: yanwei@ibp.ac.cn
Tel: 010-64888531
Address: 15 Datun Road, Chaoyang District, Beijing, 100101, China
Chinese personal homepage
- Biography
2000.09 - 2005.06 B.M., Nursing School, Peking University, Beijing, China
2005.09 - 2010.06 Ph.D., Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
2010.07 - 2014.12 Assistant Professor, State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
2014.07 - 2014.10 Visiting Scholar, Queensland Brain Institute, The University of Queensland, Brisbane, Australia
2015.08 - 2016.08 Visiting Scholar, Queensland Brain Institute, The University of Queensland, Brisbane, Australia
2015.01 - Associate Professor, State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences
- Awards
- Membership in Academies & Societies
- Research Interests
To investigate the inducing factors in protein modification (phosphosphrylation, glycation etc.), misfolding and related metabolic disorders by using molecular, cellular and animal models.
- Grants
1. NSFC General Program - “Metabolic disorder of ribose in diabetic encephalopathy and related mechanism”, 2017-2020, 600,000 RMB
2. NSFC Young Scientists Program - “The mechanism of Tau hyperphosphorylation induced by ribosylation”, 2013-2015, 230,000 RMB
- Selected Publications
1. Mou LX, Hu PD, Cao X, Chen Y, Xu Y, He T, Wei Y#, He RQ#. Comparison of bovine serum albumin glycation by ribose and fructose in vitro and in vivo. BBA Mol Basis Dis, 2022, 1868(1):166283. (#co-corresponding authors)
2. Li T*, Wei Y*, Qu M, Mou L, Miao J, Xi M, Liu Y, He R. Formaldehyde and de/methylation in age-related cognitive impairment. Genes, 2021, 12(6): 913. (* co-first authors)
3. 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)
4. 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.
5. 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)
6. 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)
7. 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.
8. 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)
9. 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)
10. 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)
11. 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.
12. 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)
13. 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)
14. 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.
15. 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.
16. 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)
17. 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)
18. 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)
(From Yan Wei, November 2, 2021)