ArticleHuman molecular genetics2015
Glycosylation of rhodopsin is necessary for its stability and incorporation into photoreceptor outer segment discs.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Glycosylation of the retina.Biochemical Society transactions · 2026Review
- Super-resolution microscopy reveals a Rab6a-dependent trafficking hub for rhodopsin at the mammalian rod photoreceptor Golgi.Biology open · 2025Article
- Super-resolution microscopy reveals a Rab6a-dependent trafficking hub for rhodopsin at the mammalian rod photoreceptor Golgi.bioRxiv : the preprint server for biology · 2025Article
- Endoplasmic reticulum stress and rhodopsin accumulation in an organoid model of Retinitis Pigmentosa carrying a RHO pathogenic variant.Stem cell research & therapy · 2025Article
- Defining proteoform-specific interactions for drug targeting in a native cell signalling environment.Nature chemistry · 2025Article
- Disease modeling and pharmacological rescue of autosomal dominant retinitis pigmentosa associated witheLife · 2024Article
- The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease.Progress in retinal and eye research · 2024Review
- Disease modeling and pharmacological rescue of autosomal dominant Retinitis Pigmentosa associated withmedRxiv : the preprint server for health sciences · 2023Article
- Posttranslational modifications of proteins in diseased retina.Frontiers in cellular neuroscience · 2023Review
- Extracellular vesicles highlight many cases of photoreceptor degeneration.Frontiers in molecular neuroscience · 2023Review
- Perspectives on Retinal Dolichol Metabolism, and Visual Deficits in Dolichol Metabolism-Associated Inherited Disorders.Advances in experimental medicine and biology · 2023Review
- Proteomic analysis of diabetic retinas.Frontiers in endocrinology · 2023Article
- AInternational journal of molecular sciences · 2022Article
- Glucose uptake by GLUT1 in photoreceptors is essential for outer segment renewal and rod photoreceptor survival.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Photoreceptor metabolic reprogramming: current understanding and therapeutic implications.Communications biology · 2021Review
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
- Retinal Degeneration Caused by Rod-Specific Dhdds Ablation Occurs without Concomitant Inhibition of Protein N-Glycosylation.iScience · 2020Article
- Lack of Overt Retinal Degeneration in a K42ECells · 2020Article
- SRD005825 Acts as a Pharmacologic Chaperone of Opsin and Promotes Survival of Photoreceptors in an Animal Model of Autosomal Dominant Retinitis Pigmentosa.Translational vision science & technology · 2019Article
- Human red and green cone opsins areThe Journal of biological chemistry · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Rhodopsin, a G-protein coupled receptor, most abundant protein in retinal rod photoreceptors, is glycosylated at asparagines-2 and 15 on its N-terminus. To understand the role of rhodopsin's glycosylation in vivo, we generated and characterized a transgenic mouse model that expresses a non-glycosylated form of rhodopsin. We show that lack of glycosylation triggers a dominant form of progressive retinal degeneration. Electron microscopic examination of retinas at postnatal day 17 revealed the presence of vacuolar structures that distorted rod photoreceptor outer segments and became more prominent with age. Expression of non-glycosylated rhodopsin alone showed that it is unstable and is regulated via ubiquitin-mediated proteasomal degradation at the base of outer segments. We observed similar vacuolization in outer segments of transgenic mice expressing human rhodopsin with a T17M mutation (hT17M), suggesting that the mechanism responsible for the degenerative process in mice expressing the non-glycosylated rhodopsin and the RHO(hT17M) mice is likely the cause of phenotype observed in retinitis pigmentosa patients carrying T17M mutation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.