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Literature summary for 1.6.3.1 extracted from

  • Chiriac, M.T.; Roesler, J.; Sindrilaru, A.; Scharffetter-Kochanek, K.; Zillikens, D.; Sitaru, C.
    NADPH oxidase is required for neutrophil-dependent autoantibody-induced tissue damage (2007), J. Pathol., 212, 56-65.
    View publication on PubMed

Application

Application Comment Organism
medicine neutrophil cytosolic factor 1-deficient mice lacking functional NADPH oxidase are resistant to skin blistering by the passive transfer of antibodies against type VII collagen. Recruitment of granulocytes into the skin is required for tissue injury, as demonstrated by the resistance to experimental blistering of wild-type mice depleted of neutrophils and of CD18-deficient mice. Granulocyte-derived NADPH oxidase is a key molecular effector engaged by pathogenic autoantibodies and provides relevant targets for prevention of tissue damage in granulocyte-mediated autoimmune diseases Mus musculus
medicine pharmacological inhibition or deficiency of human NADPH oxidase abolishes dermal-epidermal separation caused by autoantibodies and granulocytes ex vivo. Granulocyte-derived NADPH oxidase is a key molecular effector engaged by pathogenic autoantibodies and provides relevant targets for prevention of tissue damage in granulocyte-mediated autoimmune diseases Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
granulocyte
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Mus musculus
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granulocyte
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Homo sapiens
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skin
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Homo sapiens
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