Fig. 3: Ripk3D143N/D143N mice resemble Ripk3WT/WT littermates in the absence of challenge. | Cell Death & Differentiation

Fig. 3: Ripk3D143N/D143N mice resemble Ripk3WT/WT littermates in the absence of challenge.

From: The kinase domain of RIPK3 tunes its scaffolding functions

Fig. 3

A Clustered regularly interspaced short palindromic repeats (CRISPR) gene editing strategy for the generation of Ripk3D143N/D143N mice. B Ripk3WT/WT and Ripk3D143N/D143N littermates at 4 months-of-age. C Genotype distribution at E10.5 or at weaning from heterozygous Ripk3D143N/WT matings. Statistical test to compare observed versus expected genotype ratios: χ2 test for goodness of fit showed p = 0.88 at E10.5 and p = 0.02 at weaning. See Supplementary Fig. 3H for animal numbers per genotype and age. D Immunoblot of organ homogenates of littermates, n = 2 per genotype. E Quantitation of the death of mouse dermal fibroblasts (MDF) and bone marrow derived macrophages (BMDM) from Ripk3WT/WT and Ripk3D143N/D143N mice. Cells were untreated (UT) or stimulated with TNF+Smac mimetic (TS) or TS+IDN-6556 (TSI). Cell death was measured by the uptake of SYTOX Green. BMDM death was calculated as the percentage of SYTOX Green+ cells relative to the number of SPY620+ cells. Mean ± SEM from one experiment is shown. Representative of two independent experiments across three independent MDF lines, and one BMDM experiment. F Micrographs of Ripk3WT/WT and Ripk3D143N/D143N MDF after 19 h of treatment. Scale bars represents 200 µm.

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