ArticleExperimental eye research2012
Composition and proteolytic processing of corneal deposits associated with mutations in the TGFBI gene.
Article in Experimental eye research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 55 citations in OpenAlex.
- Cryo-EM structure of TGFBIp fibrils driven by a corneal dystrophy-linked mutation enables design of peptide inhibitors of aggregation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcriptome Analysis of TGFBI Knockdown vs Normal Corneal Epithelial Cells: Implications for TGFBI Corneal Dystrophy Treatment.Biochemical genetics · 2026Article
- To What Extent is Anfinsen's Thermodynamic Hypothesis Consistent With the Formation and Polymorphism of Amyloid Fibrils?Journal of molecular biology · 2025Review
- The Ins and Outs of Clusterin: Its Role in Cancer, Eye Diseases and Wound Healing.International journal of molecular sciences · 2023Review
- Clusterin, other extracellular chaperones, and eye disease.Progress in retinal and eye research · 2022Review
- Molecular mechanisms of amyloid disaggregation.Journal of advanced research · 2022Review
- Pharmaceutical modulation of the proteolytic profile of Transforming Growth Factor Beta induced protein (TGFBIp) offers a new avenue for treatment ofJournal of advanced research · 2020Article
- The serine protease HtrA1 cleaves misfolded transforming growth factor β-induced protein (TGFBIp) and induces amyloid formation.The Journal of biological chemistry · 2019Article
- Amyloid assembly and disassembly.Journal of cell science · 2018Review
- The Human Eye Proteome Project: Updates on an Emerging Proteome.Proteomics · 2018Review
- Effect of position-specific single-point mutations and biophysical characterization of amyloidogenic peptide fragments identified from lattice corneal dystrophy patients.The Biochemical journal · 2017Article
- The differential role of HTRA1 in HPV-positive and HPV-negative cervical cell line proliferation.BMC cancer · 2016Article
- Macrophage TGF-International journal of clinical medicine · 2016Article
- Determinants of amyloid fibril degradation by the PDZ protease HTRA1.Nature chemical biology · 2015Article
- Article
- Fibril Core of Transforming Growth Factor Beta-Induced Protein (TGFBIp) Facilitates Aggregation of Corneal TGFBIp.Biochemistry · 2015Article
- Development of a Transgenic Mouse with R124H Human TGFBI Mutation Associated with Granular Corneal Dystrophy Type 2.PloS one · 2015Article
- Article
- The autolysis of human HtrA1 is governed by the redox state of its N-terminal domain.Biochemistry · 2014Article
- Comparison of two phenotypically distinct lattice corneal dystrophies caused by mutations in the transforming growth factor beta induced (TGFBI) gene.Proteomics. Clinical applications · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Different types of granular corneal dystrophy (GCD) and lattice corneal dystrophy (LCD) are associated with mutations in the transforming growth factor beta induced gene (TGFBI). These dystrophies are characterized by the formation of non-amyloid granular deposits (GCDs) and amyloid (LCD type 1 and its variants) in the cornea. Typical corneal non-amyloid deposits from GCD type 2 (R124H), amyloid from a variant of LCD type 1 (V624M) and disease-free tissue controls were procured by laser capture microdissection and analyzed by tandem mass spectrometry. Label-free quantitative comparisons of deposits and controls suggested that the non-amyloid sample (R124H) specifically accumulated transforming growth factor beta induced protein (TGFBIp/keratoepithelin/βig-h3), serum amyloid P-component, clusterin, type III collagen, keratin 3, and histone H3-like protein. The amyloid (V624M) similarly accumulated serum amyloid P-component and clusterin but also a C-terminal fragment of TGFBIp containing residues Y571-R588 derived from the fourth fasciclin-1 domain (FAS1-4), apolipoprotein E and apolipoprotein A-IV. Significantly, analyses of the amyloid sample also revealed the presence of the serine protease Htr (High-temperature requirement) A1 and a number of proteolytic cleavage sites in the FAS1-4 domain of TGFBIp. These cleavage sites were consistent with the ligand binding and proteolytic activity of HtrA1 suggesting that it plays a role in the proteolytic processing of the amyloidogenic FAS1-4 domain. Taken together, the data suggest that the amyloidogenic-prone region of the fourth FAS1 domain of TGFBIp encompasses the Y571-R588 peptide and that HtrA1 is involved in the proteolytic processing of TGFBIp-derived amyloid in vivo.
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Registered trials
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