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Yan Wei, Ph.D, Associate Professor

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)

 

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Tel: 010-64889872

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Address: No 15 Datun Road, Chaoyang District, Beijing

Postcode: 100101