ArticleDisease models & mechanisms2022
Collagen (I) homotrimer potentiates the osteogenesis imperfecta (oim) mutant allele and reduces survival in male mice.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Uncoupling TGFβ1 signalling from collagen protein synthesis in Dupuytren's disease.The Journal of pathology · 2026Article
- Molecular dynamics reveals how calcium drives hetero- versus homotrimerization of type I collagen.Biophysical journal · 2026Article
- The Impact of Ageing on Fibrillar Collagens.Sub-cellular biochemistry · 2026Review
- Water and Collagen: A Mystery Yet to Unfold.Biomacromolecules · 2025Review
- Active synthesis of type I collagen homotrimer in Dupuytren's fibrosis is unaffected by anti-TNF-α treatment.JCI insight · 2025Article
- Cardiac health, type I collagen, and aging in theAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- A new Col1a1 conditional knock-in mouse model to study osteogenesis imperfecta.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- A two-step dance commits collagen to folding.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Supporting the translation of multiscale research in rare disease.Disease models & mechanisms · 2023Article
- Murine Animal Models in Osteogenesis Imperfecta: The Quest for Improving the Quality of Life.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The osteogenesis imperfecta murine (oim) model with solely homotrimeric (α1)3 type I collagen, owing to a dysfunctional α2(I) collagen chain, has a brittle bone phenotype, implying that the (α1)2(α2)1 heterotrimer is required for physiological bone function. Here, we comprehensively show, for the first time, that mice lacking the α2(I) chain do not have impaired bone biomechanical or structural properties, unlike oim homozygous mice. However, Mendelian inheritance was affected in male mice of both lines, and male mice null for the α2(I) chain exhibited age-related loss of condition. Compound heterozygotes were generated to test whether gene dosage was responsible for the less-severe phenotype of oim heterozygotes, after allelic discrimination showed that the oim mutant allele was not downregulated in heterozygotes. Compound heterozygotes had impaired bone structural properties compared to those of oim heterozygotes, albeit to a lesser extent than those of oim homozygotes. Hence, the presence of heterotrimeric type I collagen in oim heterozygotes alleviates the effect of the oim mutant allele, but a genetic interaction between homotrimeric type I collagen and the oim mutant allele leads to bone fragility.
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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.