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      Yan Wei, Ph.D., Associate Prof.

  Members of the Youth Innovation Promotion Association, CAS

  State Key Laboratory of Brain & Cognitive Sciences, IBP

  Protein modification and metabolic disorders

  E-mail: yanwei@ibp.ac.cn

  Tel: 010-64888531, Fax: 010-64875055

  Zip code: 100101

  Chinese personal homepage

Biography & Introduction


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

Research experience

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-present Associate Professor, State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences


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

Research interest

To investigate the inducing factors in protein modification (phosphosphrylation, glycation etc.), misfolding and related metabolic disorders by using molecular, cellular and animal models.

Selected publications

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, 9(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)


From Yan Wei, 2019-10-15

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Institute of Biophysics, CAS    Address: 15 Datun Road, Chaoyang District, Beijing, 100101, China
Tel:8610-64889872    Fax: 8610-64871293    E-mail: office@ibp.ac.cn