ReviewCellular signalling2017
AIPL1: A specialized chaperone for the phototransduction effector.
Review in Cellular signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Restoring Sight: The Journey of AIPL1 from Discovery to Therapy.International journal of molecular sciences · 2025Review
- Computational Evidence for Digenic Contribution ofInternational journal of molecular sciences · 2025Article
- Cyclic nucleotide phosphodiesterases as drug targets.Pharmacological reviews · 2025Review
- RNA-Seq Analysis of Trans-Differentiated ARPE-19 Cells Transduced by AAV9-AIPL1 Vectors.International journal of molecular sciences · 2023Article
- High-Quality Chromosome-Level Genome Assembly of the Corsac Fox (International journal of molecular sciences · 2023Article
- Cellular and Molecular Mechanisms of Pathogenesis Underlying Inherited Retinal Dystrophies.Biomolecules · 2023Review
- Identification of bioactive compounds fromIn silico pharmacology · 2023Article
- Leber congenital amaurosis/early-onset severe retinal dystrophy: current management and clinical trials.The British journal of ophthalmology · 2022Review
- Photoreceptor phosphodiesterase (PDE6): activation and inactivation mechanisms during visual transduction in rods and cones.Pflugers Archiv : European journal of physiology · 2021Review
- The ubiquitin-like modifier FAT10 inhibits retinal PDE6 activity and mediates its proteasomal degradation.The Journal of biological chemistry · 2020Article
- Review
- Review
- Pathogenic variants of AIPL1, MERTK, GUCY2D, and FOXE3 in Pakistani families with clinically heterogeneous eye diseases.PloS one · 2020Article
- Interaction of the tetratricopeptide repeat domain of aryl hydrocarbon receptor-interacting protein-like 1 with the regulatory Pγ subunit of phosphodiesterase 6.The Journal of biological chemistry · 2019Article
- Balancing the Photoreceptor Proteome: Proteostasis Network Therapeutics for Inherited Retinal Disease.Genes · 2019Review
- FKBP Ligands-Where We Are and Where to Go?Frontiers in pharmacology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Molecular chaperones play pivotal roles in protein folding, quality control, assembly of multimeric protein complexes, protein trafficking, stress responses, and other essential cellular processes. Retinal photoreceptor rod and cone cells have an unusually high demand for production, quality control, and trafficking of key phototransduction components, and thus, require a robust and specialized chaperone machinery to ensure the fidelity of sensing and transmission of visual signals. Misfolding and/or mistrafficking of photoreceptor proteins are known causes for debilitating blinding diseases. Phosphodiesterase 6, the effector enzyme of the phototransduction cascade, relies on a unique chaperone aryl hydrocarbon receptor (AhR)-interacting protein-like 1 (AIPL1) for its stability and function. The structure of AIPL1 and its relationship with the client remained obscure until recently. This review summarizes important recent advances in understanding the mechanisms underlying normal function of AIPL1 and the protein perturbations caused by pathogenic mutations.
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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.