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1 Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Piscataway, NJ, USA
2 Department of Medical Chemistry, Tohoku University School of Medicine, Sendai, Miyagi, Japan
3 Department of Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: brottoma{at}UMDNJ.EDU.
Sarcalumenin is a Ca2+ binding protein located in the sarcoplasmic reticulum of striated muscle cells, whose physiological function has not been fully determined yet. Using sarcalumenin knockout (sar-/-) mice, we showed that sar ablation altered store-operated Ca2+ entry (SOCE) and enhanced muscle fatigue resistance. Sar-/- mice fatigued less with treadmill exercise and intact isolated soleus and EDL muscles from sar-/- mice were more resistant to intermittent fatiguing stimulation than those from wild type mice. Enhanced SOCE was observed in the sar-/- muscles. Biochemical analysis revealed that sar-/- muscles contained significantly elevated expression of mitsugumi 29 (MG29), a synaptophysin related membrane protein located in the triad junction of skeletal muscle. Since the ablation of mg29 has been shown to cause increased fatigability and dysfunction of SOCE, the enhanced SOCE activity seen in sar-/- muscle may be correlated with the increased expression of MG29. Our data suggests that systemic ablation of sarcalumenin caused enhanced resistance to muscle fatigue by compensatory changes in Ca2+ regulatory proteins that effect SOCE.
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