A hypomorphic mouse model of dystrophic epidermolysis bullosa reveals mechanisms of disease and response to fibroblast therapy. - Wikidata - awgldk - TriplyDB

A hypomorphic mouse model of dystrophic epidermolysis bullosa reveals mechanisms of disease and response to fibroblast therapy.

A hypomorphic mouse model of dystrophic epidermolysis bullosa reveals mechanisms of disease and response to fibroblast therapy.

http://www.wikidata.org/entity/Q36512219

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Progress toward Treatment and Cure of Epidermolysis Bullosa: Summary of the DEBRA International Research Symposium EB2015 One goal, different strategies--molecular and cellular approaches for the treatment of inherited skin fragility disorders Targeted proteolysis of plectin isoform 1a accounts for hemidesmosome dysfunction in mice mimicking the dominant skin blistering disease EBS-Ogna Aminoglycosides restore full-length type VII collagen by overcoming premature termination codons: therapeutic implications for dystrophic epidermolysis bullosa.Recessive dystrophic epidermolysis bullosa results in painful small fibre neuropathy.Cell therapy in dermatology.Mechanisms of fibroblast cell therapy for dystrophic epidermolysis bullosa: high stability of collagen VII favors long-term skin integrity Bone marrow transplantation restores epidermal basement membrane protein expression and rescues epidermolysis bullosa model mice.Bone marrow transplantation for recessive dystrophic epidermolysis bullosa A COL7A1 mutation causes dystrophic epidermolysis bullosa in Rotes Höhenvieh cattle.Blister-inducing antibodies target multiple epitopes on collagen VII in mice.A mouse model of generalized non-Herlitz junctional epidermolysis bullosa.Rat model for dominant dystrophic epidermolysis bullosa: glycine substitution reduces collagen VII stability and shows gene-dosage effect Generation of 3D skin equivalents fully reconstituted from human induced pluripotent stem cells (iPSCs).Preconditioning of mesenchymal stem cells for improved transplantation efficacy in recessive dystrophic epidermolysis bullosa Genomic copy number variation in Mus musculus Losartan ameliorates dystrophic epidermolysis bullosa and uncovers new disease mechanisms Dynamic involvement of ATG5 in cellular stress responses.Novel molecular therapies for heritable skin disorders Animal models of skin disease for drug discovery.Global remodelling of cellular microenvironment due to loss of collagen VII.The transition from linear to highly branched poly(β-amino ester)s: Branching matters for gene delivery.Amelioration of epidermolysis bullosa by transfer of wild-type bone marrow cells Chemotaxis-driven disease-site targeting of therapeutic adult stem cells in dystrophic epidermolysis bullosa Autoimmunity against type VII collagen in inflammatory bowel disease Keratinocyte-/fibroblast-targeted rescue of Col7a1-disrupted mice and generation of an exact dystrophic epidermolysis bullosa model using a human COL7A1 mutation.Allogeneic blood and bone marrow cells for the treatment of severe epidermolysis bullosa: repair of the extracellular matrix.Patient-specific naturally gene-reverted induced pluripotent stem cells in recessive dystrophic epidermolysis bullosa Novel and emerging therapies in the treatment of recessive dystrophic epidermolysis bullosa.Genetic analyses of integrin signaling.Cell-extracellular matrix interactions in normal and diseased skin.Concise review: Transplantation of human hematopoietic cells for extracellular matrix protein deficiency in epidermolysis bullosa.Bone marrow transplantation in epidermolysis bullosa.The long and winding road that leads to a cure for epidermolysis bullosa.Gene therapy: pursuing restoration of dermal adhesion in recessive dystrophic epidermolysis bullosa.Treatment of hereditary epidermolysis bullosa: updates and future prospects.Inherited blistering skin diseases: underlying molecular mechanisms and emerging therapies.Trans-splicing improvement by the combined application of antisense strategies.Suppression of TGFβ and Angiogenesis by Type VII Collagen in Cutaneous SCC.Therapies for inherited skin fragility disorders.

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A hypomorphic mouse model of dystrophic epidermolysis bullosa reveals mechanisms of disease and response to fibroblast therapy.

http://www.wikidata.org/entity/Q36512219

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A hypomorphic mouse model of d ...... esponse to fibroblast therapy.

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A hypomorphic mouse model of d ...... esponse to fibroblast therapy.

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Journal of Clinical Investigation

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A hypomorphic mouse model of d ...... esponse to fibroblast therapy.

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Anja Fritsch

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Attila Braun

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Dirk Berens von Rautenfeld

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Dominik Paul

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Dominik von Elverfeldt

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Hauke Schumann

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Ingrid Hausser

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Johannes S Kern

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Michael R Bösl

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Miriam Erlacher

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P2860

Epidermolysis bullosa. II. Type VII collagen mutations and phenotype-genotype correlations in the dystrophic subtypes

Inflammation and cancer

Delayed wound repair and impaired angiogenesis in mice lacking syndecan-4

The myofibroblast: one function, multiple origins

Tenascins: regulation and putative functions during pathological stress

Proteinases of the bone morphogenetic protein-1 family convert procollagen VII to mature anchoring fibril collagen

Derivation of completely cell culture-derived mice from early-passage embryonic stem cells

TGF-beta signaling in fibroblasts modulates the oncogenic potential of adjacent epithelia

Expanding the COL7A1 mutation database: novel and recurrent mutations and unusual genotype-phenotype constellations in 41 patients with dystrophic epidermolysis bullosa.

Decreased embryonic retinoic acid synthesis results in a DiGeorge syndrome phenotype in newborn mice

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1669-1679

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10.1172/JCI34292

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5

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118

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Leena Bruckner-Tuderman

Reinhard Fässler

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2008-05-01T00:00:00Z

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18382769

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