ArticleThe Journal of investigative dermatology2014
Loss of collagen VII is associated with reduced transglutaminase 2 abundance and activity.
Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 65 citations in OpenAlex.
- Marine collagen for regenerative medicine: Structure-function advantages, limitations, and translational pathways.Bioactive materials · 2026Review
- Collagen VII Is Associated with Airway Remodeling, Honeycombing, and Fibroblast Foci in Usual Interstitial Pneumonia/Idiopathic Pulmonary Fibrosis.The American journal of pathology · 2025Article
- The Role of Fibroblasts in Dystrophic Epidermolysis Bullosa Pathogenesis and Current Treatment Approaches.JID innovations : skin science from molecules to population health · 2025Review
- Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa.International journal of molecular sciences · 2025Article
- Maintenance of chronicity signatures in fibroblasts isolated from recessive dystrophic epidermolysis bullosa chronic wound dressings under culture conditions.Biological research · 2023Article
- Collagen VII maintains proteostasis in dermal fibroblasts by scaffolding TANGO1 cargo.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy.Antibodies (Basel, Switzerland) · 2021Review
- Impaired Wound Healing, Fibrosis, and Cancer: The Paradigm of Recessive Dystrophic Epidermolysis Bullosa.International journal of molecular sciences · 2021Review
- Signatures of Dermal Fibroblasts from RDEB Pediatric Patients.International journal of molecular sciences · 2021Article
- Dystrophic Epidermolysis Bullosa: Secondary Disease Mechanisms and Disease Modifiers.Frontiers in genetics · 2021Review
- Epidermolysis Bullosa-Associated Squamous Cell Carcinoma: From Pathogenesis to Therapeutic Perspectives.International journal of molecular sciences · 2019Review
- Fibroblast activation and abnormal extracellular matrix remodelling as common hallmarks in three cancer-prone genodermatoses.The British journal of dermatology · 2019Observational
- Targeting defective proteostasis in the collagenopathies.Current opinion in chemical biology · 2019Review
- Mass Spectrometry-Based Proteomics to Define Intracellular Collagen Interactomes.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Influenza A Virus Induces Autophagosomal Targeting of Ribosomal Proteins.Molecular & cellular proteomics : MCP · 2018Article
- Combinatorial Omics Analysis Reveals Perturbed Lysosomal Homeostasis in Collagen VII-deficient Keratinocytes.Molecular & cellular proteomics : MCP · 2018Article
- Preventive effect of dietary astaxanthin on UVA-induced skin photoaging in hairless mice.PloS one · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Absence of collagen VII leads to widespread cellular and tissue phenotypes. However, the underlying molecular mechanisms are not well understood. To gain insights into cellular responses to loss of collagen VII, we undertook a quantitative disease proteomics approach. By using recessive dystrophic epidermolysis bullosa (RDEB), a skin blistering disease caused by collagen VII deficiency, as a genetic model, collagen VII-dependent differences in cellular protein abundances and protein-protein interactions were analyzed. Absence of collagen VII led to alterations of intracellular protein compositions and to perturbations in cell adhesion, protein trafficking, and the turnover pathway autophagy. A potential linker of the different cellular phenotypes is transglutaminase 2 (TGM2), a multifunctional enzyme important for protein cross-linking. TGM2 was identified as a stable interaction partner of collagen VII. In RDEB, both abundance and activity of TGM2 were reduced, accounting not only for diminished adhesion and perturbed autophagy but also for reduced cross-linking of the extracellular matrix and for decreased epidermal-dermal integrity in RDEB.
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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.