Muscle-specific protein that plays a central role in cell membrane repair by nucleating the assembly of the repair machinery at injury sites. Specifically binds phosphatidylserine. Acts as a sensor of oxidation: upon membrane damage, entry of extracellular oxidative environment results in disulfide bond formation and homooligomerization at the injury site. This oligomerization acts as a nucleation site for recruitment of TRIM72-containing vesicles to the injury site, leading to membrane patch formation. Probably acts upstream of the Ca2+-dependent membrane resealing process. Required for transport of DYSF to sites of cell injury during repair patch formation. Regulates membrane budding and exocytosis. May be involved in the regulation of the mobility of KCNB1-containing endocytic vesicles (By similarity).
Background References
1. Nagre N. et. al. TRIM72 modulates caveolar endocytosis in repair of lung cells. Am J Physiol Lung Cell Mol Physiol. 2016 Mar 1;310(5):L452-64.
2. Ishiwata-Endo H. et. al. Role of a TRIM72 ADP-ribosylation cycle in myocardial injury and membrane repair. JCI Insight. 2018 Nov 15;3(22). pii: 97898.
Western blot analysis of TRIM72 on different lysates with Mouse anti-TRIM72 antibody (HA601228) at 1/1,000 dilution.
Lane 1: HCT 116 cell lysate (20 µg/Lane) Lane 2: Mouse skeletal muscle tissue lysate (40 µg/Lane) Lane 3: Mouse heart tissue lysate (40 µg/Lane) Lane 4: Rat heart tissue lysate (40 µg/Lane) Lane 5: Rat skeletal muscle tissue lysate (40 µg/Lane)
Predicted band size: 53 kDa Observed band size: 53 kDa
Exposure time: 1 minute 40 seconds;
4-20% SDS-PAGE gel.
Proteins were transferred to a PVDF membrane and blocked with 5% NFDM/TBST for 1 hour at room temperature. The primary antibody (HA601228) at 1/1,000 dilution was used in 5% NFDM/TBST at 4℃ overnight. Goat Anti-Mouse IgG for IP, AlpSdAbs® VHH(HRP) (001-100-005) at 1/5,000 dilution was used for 1 hour at room temperature.
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