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Contains a homozygous disruption of the Stat1 gene and complete lack of functional STAT1 proteins
The JAK-STAT signaling pathway has been implicated in mediating biologic responses induced by many cytokines
Homozygous mice develop normally
Deficient immune cell response to alpha(α) and gamma(γ) interferons
Extreme susceptibility to infections by microbial pathogens and viruses
Could be used as sentinel animals for evaluating the health status of a mouse colony
Accelerated and amplified development of chemically-induced and spontaneous tumors
Useful in determining the role of a variety of cytokines in immune responses, the role of STAT1 protein in mediating interferon-dependent responses, and the roles of tumor cells and immune cells in mediating tumor cell destruction
Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
Genetic Background: 129S6 Background
Origin: The Stat1 mouse was developed in the laboratory of Robert Schreiber at the Washington University School of Medicine. The model was created by targeting the Stat1 gene in GS-1 ES cells and injecting the targeted cells into blastocysts. Heterozygotes for the mutation were produced from the chimeras and intercrossed to generate homozygotes. Taconic received stock in 1997. The mice were embryo transfer derived. The original Stat1 model (000679-M) differed from the Taconic 129S6 at two biochemical loci, Pgm1 and Gpi1. In January 2002, the original Stat1 line was backcrossed to the Taconic 129S6/SvEvTac, and animals were selected to match the Pgm1c and Gpi1b alleles of the 129S6. The selected heterozygotes were intercrossed to homozygosity. The line is maintained through incrossing of homozygous mice. This improvement makes the 129S6/SvEvTac a more perfectly matched control for the Stat1 model.
Genetics: Wild type for Nnt mutation
Color: White-Bellied Agouti
Meraz MA, White JM, Sheehan KC, Bach EA, Rodig SJ, Dighe AS, Kaplan DH, Riley JK, Greenlund AC, Campbell D, Carver-Moore K, DuBois RN, Clark R, Aguet M, Schreiber RD. (1996) Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway
. Cell, 84(3):431-442