Education

Education

1993-2000: Postdoc, Kyoto University & Osaka University Graduate School of Medicine, Japan

1989-1993: Ph.D., Graduate School of Chinese Academy of Agriculture Science, Beijing, China

1989-1992: Graduate research at the School of Medicine Chiba University, Chiba, Japan

Teaching

• Summer Undergraduate Program in Neurosciences
• Neuro 203 - Investigative Neuroscience, Graduate Students
• Neuro 250 - Molecular Neurobiology, Graduate Students
• CSI100/200 - Clinical Skills Integration/Journal club, 1^st and 2^nd year medical students

Publications

1. Li S. Sato K, and Jin M. (2026) RGR-mediated photopic visual cycle and oxidative stress: Potential mechanisms for cone vision impairment and retinal degeneration in retinitis pigmentosa linked to D1080N-IRBP.J Neurosci. 46(13): e1924252026, PMID: 41775632
    
2. Li S. and Jin M. (2024) Ablation of fatty acid transport protein-4 enhances cone survival, M-cone vision, and synthesis of cone-tropic 9-cis-retinal in rd12 mouse model of Leber congenital amaurosis.J Neurosci. 44(27):1994-23. PMC11223470
    
3. Lu C, Li S, and Jin M. (2022) Rapamycin inhibits light-induced necrosome activation occurring in wild-type, but not RPE65-null, mouse retina.Invest Ophthalmol Vis Sci. 63(13):19. PMC9769341
    
4. Li S, Gordon WC, Bazan NG, and Jin M. (2020) Inverse correlation between fatty acid transport protein 4 and vision in Leber congenital amaurosis associated with RPE65 mutation. Proc Natl Acad Sci U S A, 117: 32114-23. 
    
5. Li S, Green JF, and Jin M. (2019) Impacts of deletion and Ichthyosis prematurity syndrome-associated mutations in fatty acid transport protein-4 on the function of RPE65. FEBS Lett. 594: 540-52.
    
6. Li S, Sato K, Gordon WC, Sendtner M, Bazan NG, and Jin M. (2018) Ciliary neurotrophic factor (CNTF) protects retinal cone and rod photoreceptors by suppressing excessive formation of the visual pigments. J Biol Chem. 293: 15256-68.
    
7. Li S, Samardzija M, Yang Z, Grimm C, and Jin M. (2016) Pharmacological amelioration of cone survival and vision in a mouse model of Lebe congenital amaurosis, J Neurosci. 36:5808-19.
    
8. Lee M, Li S, Sato K, and Jin M. (2016) Interphotoreceptor retinoid-binding protein mitigates cellular oxidative stress and mitochondrial dysfunction induced by all-trans-retinal, Invest Ophthalmol Vis Sci. 57:1553-62. 
    
9. Li S, Hu J, Jin RJ, Aiyar A, Jacobson SG, Bok D, and Jin M. (2015) Temperature-sensitive retinoid isomerase activity of RPE65 mutants associated with Leber congenital amaurosis, J Biochem. 158:115-25. 
    
10. Li S, Izumi T, Hu J, Jin HH, Siddiqui AA, Jacobson SG, Bok D, and Jin M. (2014) Rescue of enzymatic function for disease-associated RPE65 proteins containing various missense mutations in non-active sites, J Biol Chem. 289:18943-56. 
     
11. Sato K, Li S, Gordon WC, He J, Liou IG, Hill JM, Travis GH, Bazan GN, and Jin M. (2013) Receptor interacting protein kinase-mediated necrosis contributes to cone and rod photoreceptor degeneration in the retina lacking interphotoreceptor retinoid-binding protein, J Neurosci. 33:17458-68.
     
12. Li S,* Yang Z,* Hu J, Gordon WC, Bazan GN, Haas AL, Bok D, and Jin M. (2013) Secretory defect and cytotoxicity: the potential disease mechanisms for the retinitis pigmentosa (RP)-associated interphotoreceptor retinoid-binding protein (IRBP), J Biol Chem. 288:11395-406 (*co-first author).
     
13. Li S, Lee J, Zhou Y, Gordon WC, Hill JM, Bazan NG, Miner JH, and Jin M. (2013) Fatty acid transport protein 4 (FATP4) prevents light-induced degeneration of cone and rod photoreceptors by inhibiting RPE65 isomerase, J Neurosci. 33:3178-89.
     
14. Guignard TJ, Jin M, Pequignot MO, Li S, Chassigneux Y, Chekroud K, Guillou L, Richard E, Hamel CP, and Brabet P (2010) FATP1 inhibits 11-cis retinol formation via interaction with the visual cycle retinoid isomerase RPE65 and lecithin:retinol acyltransferase, J Biol Chem. 285:18759-68.
     
15. Philpa AR,* Jin M,* Li S, Schindler E, Iannaccone A, Lam BL, Weleber RG, Fishman SA, Jacobson SG, Mullins R, Travis GH, and Stone EM (2009) Predicting the pathogenicity of RPE65 mutations, Hum Mutat. 30:1183-88. (*co-first author). 
     
16. Jin M, Li S, Nusinowitz S, Lloyd M, Hu J, Radu R, Bok D, and Travis GH. (2009) The role of interphotoreceptor retinoid-binding protein on the translocation of visual retinoid and survival of cone photoreceptors, J Neurosci. 29:1486-95.
     
17. Kusakabe Y, Takimoto N, Jin M, and Tsuda M. (2009) Evolution of the retinoid cycle in vertebrates, Philos Trans R Soc Lond B Biol Sci. 364:2897-910.
     
18. Jin M, Yuan Q, Li S, Travis GH. (2007) Role of LRAT on the retinoid isomerase activity and association of Rpe65 with membrane, J Biol Chem. 282:20915-24. 
     
19. Jin M, Ishida M, Katoh-Fukui Y, Tsuchiya R, Higashinakagawa T, and Arimatsu Y.  (2006) Reduced pain sensitivity in mice lacking Latexin, an inhibitor for metallocarboxypeptidases, Brain Res. 1075:117-21.
     
20. Jin M, Li S, Moghrabi WN, Sun H, and Travis GH. (2005) RPE65 is the retinoid isomerase in bovine retinal pigment epithelium, Cell 122:449-59.

Research

Keywords:
Biochemistry and molecular biology of vision, mechanisms of neurodegeneration, alleviation of retinal degeneration

Current Research:

The long-term goals of our current research are to 1) decipher the mechanisms that regulate the visual cycle in the physiological and pathological conditions, 2) identify the signaling pathways leading to retinal neurodegeneration in mouse models with aberrant visual cycle, and 3) develop viable interventions alleviating neurodegeneration caused by mutations in the visual cycle genes.

The phototransduction that converts light energy into electrical energy and neural signal starts with photoisomerization of 11-cis retinaldehyde (11cRAL) to all-trans isomer in Opsin protein, a G-protein coupled receptor in the retinal photoreceptor neurons. Since an Opsin without 11cRAL chromophore is not responsive to light, sustained vision requires continuous regeneration of the light sensitive visual pigment consisting of an 11cRAL and an Opsin protein. In vertebrate eyes, the visual pigment is generated via the visual cycle, a series of enzymatic reactions taking place in the photoreceptor neurons and the retinal pigment epithelium. Dysfunction in any proteins involved in the visual cycle causes vision impairment and retinal degenerative diseases such as Leber’s congenital amaurosis and retinitis pigmentosa. Although the visual cycle is essential for sustaining vision, its intermediates and byproducts are toxic to cells and are involved in the pathogenic mechanisms for Stargardt disease and age-related macular degeneration.

To achieve the research goals, we are currently focusing on 1) screening for new regulators of the visual cycle, 2) generation and characterization of new mouse models for retinal diseases, and 3) pharmacological rescue of photoreceptor function in mouse models of retinal degeneration. We use molecular biology, biochemistry, electrophysiology, and mouse genetics to accomplish these research projects

 Funding

• Title: IRBP in the visual cycles and retinal diseases 
  Principal Investigator (PI): M. Jin, NIH-R01EY036015
• Title: Mechanisms that regulate RPE65 isomerase in normal & blindness-associated RPE
  Principal Investigator (PI): M. Jin, NIH-R01EY028572
• Title: RPE apical proteins that regulate the visual cycle
  Principal Investigator (PI): M. Jin, NIH-R21EY028255

Committees & Administrative Responsibilities

• 2012 – present, Research Enhancement Committee/Internal Funding Review Panel
• 2013 – present, Committee on Communications
• 2014 – Present, Sabbatical Leave Review Committee
• 2015 – Present, Faculty Development and Evaluation Committee
• 2016 – Present, International Travel Review Committee