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Inducible Protein Homodimerization - argent Regulated

A, Genetic cross between Kit/MCM and R-GFP reporter mice to lineage trace c-kit-expressing cells when tamoxifen is present. B, Schematic showing tamoxifen treatment between day 1 and 6 months of age (panels c g ). H j, Tamoxifen treatment of Kit/MCM, r-GFP mice between 612 weeks of age followed by disassociation of cells from the hearts of these mice in h (white arrow in i shows rare cardiomyocyte) that is quantified in j (127,284 cardiomyocytes across two hearts, 7 were eGFP, P 0.05 versus R-GFP). M, n, Disassociated cardiomyocytes show rare but definitive myocyte labelling (white arrow which was quantified in n (225,760 cardiomyocytes from 2 myocardial infarction-injured hearts, 37 were eGFP, P 0.05 versus R-GFP).

O, p, Tamoxifen treatment between 8 and 12 weeks of age with myocardial infarction injury occurring 3 days after tamoxifen cessation. P, Average number of eGFP cardiomyocytes from histological sections taken across the entire heart ( n 2 hearts, 50 sections each) P 0.05 versus R-GFP.

All error bars represent s.e.m. K n, Tamoxifen treatment of Kit/MCM R-GFP mice between 8 and 14 weeks of age with myocardial infarction (MI) on week 10 ( n 3 mice analysed). L, Immunohistological heart section for desmin (red) and eGFP (green) with nuclei in blue (arrow shows a cardiomyocyte from the c-kit lineage).

P 0.05 versus R-GFP. F, g, Representative heart sections from Kit/MCM, r-GFP mice showing c-kit lineage cells in green and cardiomyocytes in red (desmin antibody). White arrow indicates eGFP adult cardiomyocyte ( n 3 mice analysed). C, d, Representative facs plots with c-kit antibody versus eGFP from bone marrow of Kit/MCM. R-GFP mice without ( c ) or with ( d ) tamoxifen. E, facs quantification of eGFP cells from bone marrow of these mice (average from n 2 mice for R-GFP and n 4 for Kit/MCM, r-GFP).

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