ArticleThe FEBS journal2018
Proteomic profiling of TGFBI-null mouse corneas reveals only minor changes in matrix composition supportive of TGFBI knockdown as therapy against TGFBI-linked corneal dystrophies.
Article in The FEBS journal, 2018. 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, 34 citations in OpenAlex.
- A Novel Loss-of-Function Variant inGenes · 2026Article
- Mechanobiology of Matricellular Proteins in Bladder Cancer: A Narrative Review and Bioinformatics Analysis.Biomolecules · 2026Review
- The human limbus functions as an instructive epithelial transition zone.Research square · 2026Article
- Transcriptome Analysis of TGFBI Knockdown vs Normal Corneal Epithelial Cells: Implications for TGFBI Corneal Dystrophy Treatment.Biochemical genetics · 2026Article
- [Integrating Bioinformatics and Machine Learning Algorithms to Screen Inflammatory Biomarkers for Atrial Fibrillation and Experimental Validation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Article
- Precise CRISPR-Mediated Editing of theInternational journal of molecular sciences · 2026Article
- Essential Role of CD63 in Maintaining Corneal Epithelial Identity in the Human Limbus.Investigative ophthalmology & visual science · 2026Article
- Transcriptomic landscape of quiescent and proliferating human corneal stromal fibroblasts.Experimental eye research · 2024Article
- The coordinated activities of collagen VI and XII in maintenance of tissue structure, function and repair: evidence for a physical interaction.Frontiers in molecular biosciences · 2024Article
- Potential underlying genetic associations between keratoconus and diabetes mellitus.Advances in ophthalmology practice and research · 2021Article
- Compound heterozygous mutations in TGFBI cause a severe phenotype of granular corneal dystrophy type 2.Scientific reports · 2021Article
- Characterization of a pluripotent stem cell-derived matrix with powerful osteoregenerative capabilities.Nature communications · 2020Article
- Investigation of TGFBI (transforming growth factor beta-induced) Gene Mutations in Families with Granular Corneal Dystrophy Type 1 in the Konya Region.Turkish journal of ophthalmology · 2020Article
- Label-Free Quantitative Proteomics Distinguishes General and Site-Specific Host Responses to Pseudomonas aeruginosa Infection at the Ocular Surface.Proteomics · 2020Article
- The serine protease HtrA1 cleaves misfolded transforming growth factor β-induced protein (TGFBIp) and induces amyloid formation.The Journal of biological chemistry · 2019Article
- Fascinating Fasciclins: A Surprisingly Widespread Family of Proteins that Mediate Interactions between the Cell Exterior and the Cell Surface.International journal of molecular sciences · 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
10 authors at 4 institutions in 2 countries.
Funding
Abstract
TGFBIp is a constituent of the extracellular matrix in many human tissues including the cornea, where it is one of the most abundant proteins expressed. TGFBIp interacts with Type I, II, IV, VI, and XII collagens as well as several members of the integrin family, suggesting it plays an important role in maintaining structural integrity and possibly corneal transparency as well. Significantly, more than 60 point mutations within the TGFBI gene have been reported to result in aberrant TGFBIp folding and aggregation in the cornea, resulting in severe visual impairment and blindness. Several studies have focused on targeting TGFBIp in the cornea as a therapeutic approach to treat TGFBI-linked corneal dystrophies, but the effect of this approach on corneal homeostasis and matrix integrity remained unknown. In the current study, we evaluated the histological and proteomic profiles of corneas from TGFBI-deficient mice as well as potential redundant functions of the paralogous protein POSTN. The absence of TGFBIp in mouse corneas did not grossly affect the collagen scaffold, and POSTN is unable to compensate for loss of TGFBIp. Proteomic comparison of wild-type and TGFBI
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.