ArticleThe Journal of investigative dermatology2010
A mouse model of generalized non-Herlitz junctional epidermolysis bullosa.
Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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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.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- High-frequency Ultrasound Reveals Epidermal-dermal Structural Alterations in an Experimental Model of Epidermolysis Bullosa.Acta dermato-venereologica · 2026Article
- Trametinib-Induced Epidermal Thinning Accelerates a Mouse Model of Junctional Epidermolysis Bullosa.Biomolecules · 2023Article
- Seven naturally variant loci serve as genetic modifiers of Lamc2jeb induced non-Herlitz junctional Epidermolysis Bullosa in mice.PloS one · 2023Article
- Functional analysis of Collagen 17a1: A genetic modifier of junctional epidermolysis bullosa in mice.PloS one · 2023Article
- Dystonin modifiers of junctional epidermolysis bullosa and models of epidermolysis bullosa simplex without dystonia musculorum.PloS one · 2023Article
- Mouse strain-specific polymorphic provirus functions as cis-regulatory element leading to epigenomic and transcriptomic variations.Nature communications · 2021Article
- The dysfunction of BP180/collagen XVII in keratinocytes promotes melanoma progression.Oncogene · 2019Article
- Mouse germ line mutations due to retrotransposon insertions.Mobile DNA · 2019Review
- Unraveling the ECM-Immune Cell Crosstalk in Skin Diseases.Frontiers in cell and developmental biology · 2019Review
- Skin fragility in the wild-derived, inbred mouse strain Mus pahari/EiJ.Experimental and molecular pathology · 2017Article
- A new mouse model of junctional epidermolysis bullosa: the LAMB3 628G>A knockin mouse.The Journal of investigative dermatology · 2015Article
- Cell therapy in dermatology.Cold Spring Harbor perspectives in medicine · 2014Review
- Molecular identification of collagen 17a1 as a major genetic modifier of laminin gamma 2 mutation-induced junctional epidermolysis bullosa in mice.PLoS genetics · 2014Article
- Palifermin for the protection and regeneration of epithelial tissues following injury: new findings in basic research and pre-clinical models.Journal of cellular and molecular medicine · 2013Review
- Animal models of skin disease for drug discovery.Expert opinion on drug discovery · 2013Review
- A direct method to determine the strength of the dermal-epidermal junction in a mouse model for epidermolysis bullosa.Experimental dermatology · 2012Article
- Keratinocyte-targeted expression of human laminin γ2 rescues skin blistering and early lethality of laminin γ2 deficient mice.PloS one · 2012Article
- Genetic analyses of integrin signaling.Cold Spring Harbor perspectives in biology · 2011Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Epidermolysis bullosa (EB) is a class of intractable, rare, genetic disorders characterized by fragile skin and blister formation as a result of dermal-epidermal mechanical instability. EB presents with considerable clinical and molecular heterogeneity. Viable animal models of junctional EB (JEB), that both mimic the human disease and survive beyond the neonatal period, are needed. We identified a spontaneous, autosomal recessive mutation (Lamc2(jeb)) due to a murine leukemia virus long terminal repeat insertion in Lamc2 (laminin gamma2 gene) that results in a hypomorphic allele with reduced levels of LAMC2 protein. These mutant mice develop a progressive blistering disease validated at the gross and microscopic levels to closely resemble generalized non-Herlitz JEB. The Lamc2(jeb) mice display additional extracutaneous features such as loss of bone mineralization and abnormal teeth, as well as a respiratory phenotype that is recognized but not as well characterized in humans. This model faithfully recapitulates human JEB and provides an important preclinical tool to test therapeutic approaches.
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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.