ArticleMolecular vision2009
Overexpression of CERKL, a gene responsible for retinitis pigmentosa in humans, protects cells from apoptosis induced by oxidative stress.
Article in Molecular vision, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Trial
- Outer retinal tubulation associated with photoreceptor degeneration.Progress in retinal and eye research · 2026Review
- Article
- Ceramide kinase-mediated C1P metabolism attenuates acute liver injury by inhibiting the interaction between KEAP1 and NRF2.Experimental & molecular medicine · 2024Article
- Oxidative stress in the eye and its role in the pathophysiology of ocular diseases.Redox biology · 2023Review
- Exacerbated response to oxidative stress in the Retinitis Pigmentosa CerklRedox biology · 2023Article
- Metallothioneins, a Part of the Retinal Endogenous Protective System in Various Ocular Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Genetic dissection of non-syndromic retinitis pigmentosa.Indian journal of ophthalmology · 2022Review
- Deuterated docosahexaenoic acid protects against oxidative stress and geographic atrophy-like retinal degeneration in a mouse model with iron overload.Aging cell · 2022Article
- Overexpression of CERKL Protects Retinal Pigment Epithelium Mitochondria from Oxidative Stress Effects.Antioxidants (Basel, Switzerland) · 2021Article
- CERKL is upregulated in cutaneous squamous cell carcinoma and maintains cellular sphingolipids and resistance to oxidative stress.The British journal of dermatology · 2021Article
- Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa.Antioxidants (Basel, Switzerland) · 2021Review
- Transcriptomic analysis of the liver in aged laying hens with different intensity of brown eggshell color.Animal bioscience · 2021Article
- A New Cerkl Mouse Model Generated by CRISPR-Cas9 Shows Progressive Retinal Degeneration and Altered Morphological and Electrophysiological Phenotype.Investigative ophthalmology & visual science · 2020Article
- The Relevance of Oxidative Stress in the Pathogenesis and Therapy of Retinal Dystrophies.Antioxidants (Basel, Switzerland) · 2020Review
- Deciphering retinal diseases through the generation of three dimensional stem cell-derived organoids: Concise Review.Stem cells (Dayton, Ohio) · 2019Review
- Article
- Article
- Sphingolipids as Emerging Mediators in Retina Degeneration.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeRetinitis pigmentosa (RP), a retinal neurodegenerative disorder characterized by apoptosis of photoreceptor cells, is caused by mutations in many different genes. We analyzed the RP gene ceramide kinase-like (CERKL) to determine CERKL function and contribution to pathogenesis.
methodsRT-PCR was performed to characterize CERKL expression in many human adult and fetal tissues, including retina. We analyzed the protein subcellular localization by confocal microscopy and further verified it by sucrose gradients. We performed lipid kinase activity assays. And finally, we studied the effects on cell apoptosis after CERKL overexpression in transiently transfected cultured cells by propidium iodide staining and poly-(ADP-ribose)-polymerase (PARP) caspase-dependent cleavage.
resultsCERKL transcripts underwent alternative splicing. In the human retina, four different CERKL isoforms of 532, 558, 419, and 463 amino acids were expressed. CERKL proteins were mainly localized in the endoplasmic reticulum and Golgi compartments, but they also shifted localization to nuclei and nucleoli. We also found that CERKL prevented cells from entering apoptosis induced by oxidative-stress conditions.
conclusionsCERKL remains a unique orphan lipid kinase in that no candidate substrate has been identified after intense research. The dynamic localization of CERKL suggests multiple sites of action. Remarkably, CERKL (but not the RP R257X mutant) exerts a protective role in cells against oxidative stress, consistent with RP mutations impairing the normal protein function in photoreceptors and thus tilting the balance toward apoptosis. These results provide valuable insights into the molecular mechanisms causing retinal degeneration.
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Identifiers
19158957PMC2628313W1726278660What OpenQuestion holds
Registered trials
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