2.3.1.135 Blindness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438524&form=6&db=m Low prevalence of lecithin retinol acyltransferase mutations in patients with Leber congenital amaurosis and autosomal recessive retinitis pigmentosa. causal interaction,ongoing research,unassigned 2,2,0 2.3.1.135 Blindness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21555576&form=6&db=m Cone opsin determines the time course of cone photoreceptor degeneration in Leber congenital amaurosis. causal interaction,unassigned 2,0 2.3.1.135 Blindness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22531707&form=6&db=m Chemical chaperone TUDCA preserves cone photoreceptors in a mouse model of Leber congenital amaurosis. unassigned - 2.3.1.135 Blindness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24664772&form=6&db=m Pathophysilogical mechanism and treatment strategies for leber congenital amaurosis. causal interaction,unassigned 3,0 2.3.1.135 Blindness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25416279&form=6&db=m Genetic deletion of S-opsin prevents rapid cone degeneration in a mouse model of Leber congenital amaurosis. causal interaction,unassigned 3,0 2.3.1.135 Blindness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32084365&form=6&db=m Deletion of M-opsin prevents "M cone" degeneration in a mouse model of Leber congenital amaurosis. causal interaction,unassigned 2,0 2.3.1.135 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9989277&form=6&db=m Reduced lecithin:retinol acyl transferase activity in cultured squamous cell carcinoma lines results in increased substrate-driven retinoic acid synthesis. ongoing research,unassigned 3,0 2.3.1.135 Carcinoma, Squamous Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9989277&form=6&db=m Reduced lecithin:retinol acyl transferase activity in cultured squamous cell carcinoma lines results in increased substrate-driven retinoic acid synthesis. ongoing research,unassigned 3,0 2.3.1.135 Hypercholesterolemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25906639&form=6&db=m Asteroid hyalosis--current state of knowledge. unassigned - 2.3.1.135 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25906639&form=6&db=m Asteroid hyalosis--current state of knowledge. unassigned - 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438524&form=6&db=m Low prevalence of lecithin retinol acyltransferase mutations in patients with Leber congenital amaurosis and autosomal recessive retinitis pigmentosa. causal interaction,ongoing research,unassigned 2,2,0 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21555576&form=6&db=m Cone opsin determines the time course of cone photoreceptor degeneration in Leber congenital amaurosis. causal interaction,unassigned 2,0 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22531707&form=6&db=m Chemical chaperone TUDCA preserves cone photoreceptors in a mouse model of Leber congenital amaurosis. unassigned - 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24664772&form=6&db=m Pathophysilogical mechanism and treatment strategies for leber congenital amaurosis. causal interaction,unassigned 3,0 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25416279&form=6&db=m Genetic deletion of S-opsin prevents rapid cone degeneration in a mouse model of Leber congenital amaurosis. causal interaction,unassigned 3,0 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25906639&form=6&db=m Asteroid hyalosis--current state of knowledge. unassigned - 2.3.1.135 Leber Congenital Amaurosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32084365&form=6&db=m Deletion of M-opsin prevents "M cone" degeneration in a mouse model of Leber congenital amaurosis. causal interaction,unassigned 2,0 2.3.1.135 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24433184&form=6&db=m Lecithin retinol acyltransferase as a potential prognostic marker for malignant melanoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,2,4 2.3.1.135 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25236354&form=6&db=m Knockdown of lecithin retinol acyltransferase increases all-trans retinoic acid levels and restores retinoid sensitivity in malignant melanoma cells. ongoing research,unassigned 3,0 2.3.1.135 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24433184&form=6&db=m Lecithin retinol acyltransferase as a potential prognostic marker for malignant melanoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,2,4 2.3.1.135 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12620121&form=6&db=m Evolutionary history, structural features and biochemical diversity of the NlpC/P60 superfamily of enzymes. unassigned - 2.3.1.135 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15161698&form=6&db=m Reduced lecithin: retinol acyltransferase expression correlates with increased pathologic tumor stage in bladder cancer. causal interaction,diagnostic usage,unassigned 3,2,0 2.3.1.135 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20610477&form=6&db=m Expression of the interleukin-4 receptor alpha in human conjunctival epithelial cells. unassigned - 2.3.1.135 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28465473&form=6&db=m Platelet-derived growth factor receptor ? in hepatocellular carcinoma is a prognostic marker independent of underlying liver cirrhosis. causal interaction,diagnostic usage,therapeutic application,unassigned 3,4,1,0 2.3.1.135 Nevus, Pigmented http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24433184&form=6&db=m Lecithin retinol acyltransferase as a potential prognostic marker for malignant melanoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,2,4 2.3.1.135 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30967641&form=6&db=m The association of lecithin retinol acyltransferase and the 25(OH)D receptor with pediatric overweight and obesity. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 2.3.1.135 Overweight http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30967641&form=6&db=m The association of lecithin retinol acyltransferase and the 25(OH)D receptor with pediatric overweight and obesity. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 2.3.1.135 Pediatric Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30967641&form=6&db=m The association of lecithin retinol acyltransferase and the 25(OH)D receptor with pediatric overweight and obesity. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 2.3.1.135 Retinal Degeneration http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11133845&form=6&db=m Genomic organization and mutation analysis of the gene encoding lecithin retinol acyltransferase in human retinal pigment epithelium. ongoing research,unassigned 2,0 2.3.1.135 Retinal Degeneration http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20404157&form=6&db=m Palmitoylation stabilizes unliganded rod opsin. diagnostic usage,ongoing research,unassigned 3,2,0 2.3.1.135 Retinal Dystrophies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11381255&form=6&db=m Mutations in the gene encoding lecithin retinol acyltransferase are associated with early-onset severe retinal dystrophy. causal interaction,unassigned 3,0 2.3.1.135 Retinal Dystrophies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21555576&form=6&db=m Cone opsin determines the time course of cone photoreceptor degeneration in Leber congenital amaurosis. causal interaction,unassigned 2,0 2.3.1.135 Retinal Dystrophies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22570351&form=6&db=m Early onset retinal dystrophy due to mutations in LRAT: molecular analysis and detailed phenotypic study. causal interaction,unassigned 4,0 2.3.1.135 Retinal Dystrophies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24664772&form=6&db=m Pathophysilogical mechanism and treatment strategies for leber congenital amaurosis. causal interaction,unassigned 3,0 2.3.1.135 Retinitis Pigmentosa http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438524&form=6&db=m Low prevalence of lecithin retinol acyltransferase mutations in patients with Leber congenital amaurosis and autosomal recessive retinitis pigmentosa. causal interaction,ongoing research,unassigned 2,2,0 2.3.1.135 Retinitis Pigmentosa http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25906639&form=6&db=m Asteroid hyalosis--current state of knowledge. unassigned - 2.3.1.135 Retinitis Pigmentosa http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29973277&form=6&db=m A novel LRAT mutation affecting splicing in a family with early onset retinitis pigmentosa. causal interaction,ongoing research,unassigned 2,1,0 2.3.1.135 Urinary Bladder Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15161698&form=6&db=m Reduced lecithin: retinol acyltransferase expression correlates with increased pathologic tumor stage in bladder cancer. causal interaction,diagnostic usage,unassigned 3,2,0