Craig Crosson
Affiliations: | Medical University of South Carolina, Charleston, SC, United States |
Area:
Molecular Biology, Cell BiologyGoogle:
"Craig Crosson"Children
Sign in to add trainee| Todd W. Shearer | grad student | 2001 | MUSC |
| Norris A. Whitlock | grad student | 2003 | MUSC |
| Oday Alsarraf | grad student | 2014 | MUSC |
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Publications
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| Fan J, Liu J, Liu J, et al. (2021) Evidence for ceramide induced cytotoxicity in retinal ganglion cells. Experimental Eye Research. 108762 |
| Desjardins D, Liu Y, Crosson CE, et al. (2016) Histone Deacetylase Inhibition Restores Retinal Pigment Epithelium Function in Hyperglycemia. Plos One. 11: e0162596 |
| Fan J, Wu BX, Crosson CE. (2016) Suppression of Acid Sphingomyelinase Protects the Retina from Ischemic Injury. Investigative Ophthalmology & Visual Science. 57: 4476-4484 |
| Fan J, Alsarraf O, Chou CJ, et al. (2016) Ischemic Preconditioning, Retinal Neuroprotection and Histone Deacetylase Activities. Experimental Eye Research |
| Wu BX, Fan J, Boyer NP, et al. (2015) Lack of Acid Sphingomyelinase Induces Age-Related Retinal Degeneration. Plos One. 10: e0133032 |
| Dahrouj M, Desjardins DM, Liu Y, et al. (2015) Receptor mediated disruption of retinal pigment epithelium function in acute glycated-albumin exposure. Experimental Eye Research. 137: 50-6 |
| Alsarraf O, Fan J, Dahrouj M, et al. (2014) Acetylation preserves retinal ganglion cell structure and function in a chronic model of ocular hypertension. Investigative Ophthalmology & Visual Science. 55: 7486-93 |
| Alsarraf O, Fan J, Dahrouj M, et al. (2014) Acetylation: a lysine modification with neuroprotective effects in ischemic retinal degeneration. Experimental Eye Research. 127: 124-31 |
| Sharif NA, Katoli P, Scott D, et al. (2014) FR-190997, a nonpeptide bradykinin B2-receptor partial agonist, is a potent and efficacious intraocular pressure lowering agent in ocular hypertensive cynomolgus monkeys. Drug Development Research. 75: 211-23 |
| Barnwell E, Padmaraju V, Baranello R, et al. (2014) Evidence of a novel mechanism for partial γ-secretase inhibition induced paradoxical increase in secreted amyloid β protein. Plos One. 9: e91531 |