2014 11:01:21 AM

Minghao Jin, Ph.D.

Professor of Neuroscience and Ophthalmology

Neuroscience Center of Excellence
School of Medicine, LSU Health
2020 Gravier St. New Orleans, LA 70112

Tel: 504-568-2141

FAX: 504-568-5801


In The News

Dr. Jin, has identified a protein that protects retinal photoreceptor cells from degeneration  caused by light damage. This result may provide a new therapeutic target for both an inherited retinal degenerative disease and age-related macular degeneration. (Li, S, et al., “Fatty Acid Transport Protein 4 (FATP4) Prevents Light-Induced Degeneration of Cone and Rod Photoreceptors by Inhibiting RPE65 Isomerase” J Neurosci. 2013 Feb 13;33(7):3178-89)



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


  • 2020-current: Professor of Ophthalmology and Neuroscience
     Neuroscience Center of Excellence, School of Medicine LSUHSC, New Orleans, LA
  • 2014-2019: Associate Professor of Ophthalmology and Neuroscience
    Neuroscience Center of Excellence, School of Medicine LSUHSC, New Orleans, LA
  • 2008-2014: Assistant Professor of Ophthalmology and Neuroscience
    Neuroscience Center of Excellence, School of Medicine LSUHSC, New Orleans, LA
  • 2001-2008: Assistant and Associate Research Professor in Ophthalmology
    Jules Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA
  • 2000-2001: Education and Science Instructor,
    Gunma University School of Medicine, Japan


  • 2014: The Morino Foundation for Molecular Science Travel Award
  • 2005: Goho Life Science International Foundation Award
  • 2004: CAAS-Sponsored Second-Class Outstanding Scientist
  • 1997-2000: Japan Science and Technology Agency Scholarship
  • 1992-1994: Education Ministry of Japan-Sponsored Overseas Fellowship

Research Interests

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



Teaching Activities

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

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

Selected Publications


  1. 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 mutationProc Natl Acad Sci U S A, 117: 32114-23.
  2. 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 RPE65FEBS Lett. 594: 540-52.
  3. 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 pigmentsJ Biol Chem293: 15256-68.
  4. Li S, Samardzija M, Yang Z, Grimm C, and Jin M. (2016) Pharmacological amelioration of cone survival and vision in a mouse model for Leber congenital amaurosisJ Neurosci 36:5808-19.
  5. 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-retinalInvest Ophthalmol Vis Sci 57:1553-62. 
  6. Jin M, Li S, Hu J, Jin HH, Jacobson SG, and Bok D. (2016) Functional rescue of retinal degeneration-associated mutant RPE65 proteinsAdv Exp Med Biol 854:525-32.
  7. 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 amaurosisJ Biochem 158:115-25. 
  8. 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 sitesJ Biol Chem 289:18943-56. 
  9. 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 proteinJ Neurosci 33:17458-68.
  10.  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).
  11. 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 isomeraseJ Neurosci 33:3178-89.
  12. Kawaguchi R, Yu J, Ter-Stepanian M, Zhong M, Cheng G, Yuan Q, Jin M, Travis GH, Ong D, Sun H. (2011) Receptor-mediated cellular uptake mechanism that couples to intracellular storageACS Chem Biol 6:1041-51.
  13. 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 acyltransferaseJ Biol Chem 285:18759-68.
  14. 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 mutationsHum Mutat 30:1183-88. (*co-first author). 
  15. 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 photoreceptorsJ Neurosci 29:1486-95. 
  16. Kusakabe Y, Takimoto N, Jin M, and Tsuda M. (2009) Evolution of the retinoid cycle in vertebratesPhilos Trans R Soc Lond B Biol Sci 364:2897-910.
  17. Jin M, Yuan Q, Li S, Travis GH. (2007) Role of LRAT on the retinoid isomerase activity and association of Rpe65 with membraneJ Biol Chem 282:20915-24. 
  18. 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 metallocarboxypeptidasesBrain Res 1075:117-21. 
  19. Kaschula CH, Jin M, Desmond-Smith NS, Li S, and Travis GH. (2006) Acyl CoA: retinol acyltransferase (ARAT) activity is present in bovine retinal pigment epitheliumExp Eye Res 82:111-21.
  20. Jin M, Li S, Moghrabi WN, Sun H, and Travis GH. (2005) RPE65 is the retinoid isomerase in bovine retinal pigment epitheliumCell 122:449-59.


Additional Info


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

Additional Info


Regulation of normal and Leber congenital amaurosis-associated RPE65s; Investigator: M. Jin, NIH-1R01EY021208-01A1