Fig. 1From: GRAF1 deficiency blunts sarcolemmal injury repair and exacerbates cardiac and skeletal muscle pathology in dystrophin-deficient miceGRAF1 accumulates at PM injury sites. a A 72-h differentiated C2C12 myoblast cut with a scalpel blade was fixed 2Â min post-injury and stained for GRAF1 (red). Note accumulation of GRAF1 at the site of injury. F-actin and nuclei were counterstained with phalloidin (green) and DAPI (blue), respectively. b GRAF1 (red) co-localizes with the membrane fusion/repair protein, annexin A1 (green) at site of microinjection needle-mediated PM puncture in cultured myoblasts. Cells were fixed and stained 2Â min after injury. c mCherry-GRAF1 labeled myofibers were laser damaged, and GRAF1 localization was monitored over time. Note that visible accumulation of GRAF1 at the site of injury (denoted by asterisk) by 100Â s post-injury. d Immunohistochemical analysis of GRAF1 expression (red) in control and saponin-treated cultured adult rat ventricular cardiomyocytes. Note that the translocation of GRAF1 to the PM of saponin-treated cells (white arrows). Nuclei are counterstained with DAPI (blue)Back to article page