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. 2003 May;14(5):2151–2162. doi: 10.1091/mbc.E02-07-0451

Figure 6.

Figure 6.

Activation of MyoD DRR during muscle regeneration requires MyoD-CArG element. To study DRR function during muscle regeneration, we generated transgenic mice carrying either 17.11wt or 17.11mut transgene (DRR-PRR-β-galactosidase) and carried out regeneration experiments. Muscle regeneration was induced in the tibialis anterior (TA) after fiber destruction with the snake toxin, notexin, as described in MATERIALS AND METHODS. At different times thereafter, injured TA muscles were analyzed for the activity of the MyoD DRR reporter activity by β-galactosidase activity (A) and for the expression of SRF and MyoD by Western blotting (B). (A) β-Galactosidase activity normalized per milligram protein at different days after muscle injury from mice carrying the wild-type (clear boxes) or mutated (dark boxes) MyoD-DRR reporter gene. The results shown are the average from two to three mice from independent experiments for each time point. (B) Western blot analysis of SRF (top panel) and MyoD (bottom panel) endogenous protein levels in injured TA muscle from 17.11m transgenic mice at different time after notexin injection.