Fig 1: Tamoxifen-inducible cardiac-specific disruption of Med1 (TmcsMed1-/-) in adult mice causes dilated cardiomyopathy.(A) Relative Med1 mRNA expression in Med1fl/fl and TmcsMed1-/- mouse heart, liver and kidney. (B) Western blot analysis of Med1 in TmMed1fl/fl and TmcsMed1-/- hearts. Crude nuclear extracts from the heart tissues of appropriate mice were prepared as described (see Materials and Methods). They were then Western immunoblotted and probed with an anti-Med1 antibody (Abcam ab64965) and the protein bands were quantified using ImageJ software. The data were normalized to ß-actin bands. Note that in the experiments shown in (A) to (H), mice were killed 14 days after first tamoxifen injection. (C) Representative photographs of adult hearts after tamoxifen-inducible heart-specific Cre mediated Med1 deletion. It is evident that TmcsMed-/- mouse heart is flaccid and flabby. Lower panel in (C) shows cross sections of TmcsMed1-/- and the littermate control hearts stained with H&E. (D and E) Representative profiles of M-mode echocardiographic analyses of TmcsMed1-/- and littermate mice. (F) and (G) represent ejection fraction and fractional shortening respectively. Data were derived from (D) and (E). (H), relative mRNA levels of BNP (Nppb) in Med1 fl/fl and TmcsMed1-/- mouse hearts. (I), survival curve. 13 mice for each group of Med1fl/fl and TmcsMed1-/- were used for the generation of survival curve. The mice survival time was between 13 and 28 days, and the day of initial injection of Tamoxifen was counted as day 1. Results are expressed as the mean ±SD. *p<0.05, **p<0.01.
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