Mice with targeted tyrosine kinase, lyn, disruption
AssigneeLudwig Institute for Cancer Research
InventorsMargaret L. Hibbs, Ashley R. Dunn, Dianne Graill, George Hodgson, David M. Tarlington, Jane Armes
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Abstract
A non-human animal carrying a disruption of a gene encoding a lyn protein tyrosine kinase provides a convenient system for the study of diseases associated with or caused by lyn deficiency, and for the testing of therapeutic agents for the treatment or prevention of diseases which include autoimmune diseases, allergy, asthma and malignant disease.
Claims22
A transgenic mouse carrying a disruption in both alleles of a gene encoding a protein tyrosine kinase, lyn, such that expression of said tyrosine kinase is at a non-existent level, wherein the disruption causes said mouse to display a phenotype characterized by lyn deficiency which results in an autoimmune disease in said mouse, and at least one symptom selected from the group consisting of;
- depletion of lymphoid tissue with age progression, extramedullary hematopoiesis, expansion of myeloid cells, glomerulonephritis, and defective IgE-mediated anaphylactic response.
A transgenic mouse carrying a disruption in both alleles of a gene encoding a protein tyrosine kinase, lyn, such that expression of said tyrosine kinase is at a non-existent level, wherein the disruption causes said mouse to display a phenotype characterized by lyn deficiency which results in impaired B cell function and/or pancytopaenia in said mouse.
A transgenic mouse carrying a disruption in both alleles of a gene encoding a protein tyrosine kinase, lyn, such that expression of the tyrosine kinase is at a non-existent level, wherein the disruption causes said mouse to display a phenotype characterized by lyn deficiency which results in a depletion of lymphoid tissue in said mouse.
A transgenic mouse carrying a disruption in both alleles of a gene encoding a protein tyrosine kinase, lyn, such that expression of the tyrosine kinase is at a non-existent level, wherein the disruption causes said mouse to display a phenotype characterized by lyn deficiency which results in a disease characterized by a malignancy of myeloid origin in said mouse.
A transgenic mouse carrying a disruption in both alleles of a gene encoding a protein tyrosine kinase, lyn, such that expression of the tyrosine kinase is at a non-existent level, wherein the disruption causes said mouse to display a phenotype characterized by lyn deficiency, which results in defective IgE anaphylactic response in said mouse.
Dependencies are inferred from the claim text.