Travis, Gabriel H. - University of California, Los Angeles

个人简介

Gabriel H. Travis is a biochemist and molecular biologist who has been on the faculty at UCLA in Ophthalmology and Biological Chemistry since 2001. Dr. Travis earned his BS degree in chemistry at UCLA, and his MD at UCLA School of Medicine. After completing a residency in neurology, Dr. Travis left clinical medicine and devote himself full-time to basic research. He completed a postdoctoral fellowship at the UCLA Molecular Biology Institute in 1984 and a second postdoctoral fellowship at Scripps Research Institute in 1989. He then took a faculty position in Neuroscience at UT Southwestern Medical Center in Dallas, where he remained until moving to UCLA. Dr. Travis currently directs a research group that studies retinoid metabolism in photoreceptor cells, and the mechanisms of inherited blinding diseases.

研究领域

Visual perception begins when a photon is captured by an opsin pigment in a rod or cone cell. This causes photoisomerization of the retinaldehyde chromophore from 11cRAL to atRAL, converting opsin to its signaling state. Shortly after, the active opsin decays, releasing free atRAL. Sensitivity is only restored to the resulting apo-opsin when it combines with another 11cRAL to form a new pigment. Our laboratory is interested in the biochemical processes that convert atRAL back to 11cRAL. The genes for several proteins of the visual cycle are affected in human inherited retinal and macular degenerations. We are working to understand what these proteins normally do for a living, and how loss of function causes blindness in people with disease-causing mutations. We are also interested in how the visual opsins maintain light sensitivity under daylight conditions where the photon fluxes and hence chromophore-consumption rates are millions-fold higher than at night. We have discovered several processes that are hugely stimulated by visible light. The action spectra for these light-induced molecular events provides interesting clues. We have several exciting projects open to study how natural light exposure affects the dynamics of visual retinoids. Our lab employs a wide range of methodologies and makes extensive use of genetically modified mice.

近期论文

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Kaylor JJ, et al. (2015) Diacylglycerol O-acyltransferase type-1 synthesizes retinyl esters in the retina and retinal pigment epithelium. PloS one 10(5):e0125921. Kaylor JJ, et al. (2014) Identification of the 11-cis-specific retinyl-ester synthase in retinal Muller cells as multifunctional O-acyltransferase (MFAT). Proc Natl Acad Sci U S A 111(20):7302-7307. Sato K, et al. (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(44):17458-17468. Kaylor JJ, et al. (2013) Identification of DES1 as a vitamin A isomerase in Muller glial cells of the retina. Nature chemical biology 9(1):30-36. Mullins RF, et al. (2012) Autosomal recessive retinitis pigmentosa due to ABCA4 mutations: clinical, pathologic, and molecular characterization. Invest Ophthalmol Vis Sci 53(4):1883-1894. Radu RA, et al. (2011) Complement system dysregulation and inflammation in the retinal pigment epithelium of a mouse model for Stargardt macular degeneration. J Biol Chem 286(21):18593-18601. Kawaguchi R, et al. (2011) Receptor-mediated cellular uptake mechanism that couples to intracellular storage. ACS chemical biology 6(10):1041-1051. Blakeley LR, et al. (2011) Rod outer segment retinol formation is independent of Abca4, arrestin, rhodopsin kinase, and rhodopsin palmitylation. Invest Ophthalmol Vis Sci 52(6):3483-3491. Yuan Q, et al. (2010) Rpe65 isomerase associates with membranes through an electrostatic interaction with acidic phospholipid headgroups. J Biol Chem 285(2):988-999. Travis GH, Kaylor J, & Yuan Q (2010) Analysis of the retinoid isomerase activities in the retinal pigment epithelium and retina. Methods Mol Biol 652:329-339.