“…On the other hand calpain activity could be also negatively regulated by phosphorylation through PKA or its endogenous inhibitor calpastatin (Melloni et al, 1984;Inomata et al, 1988;Saido et al, 1992;Croall and McGrody, 1994;Moldoveanu et al, 2001;Shiraha et al, 2002;Dedieu et al, 2003(a)). The calpain family is thought to be involved in a range of various diseases such as cataract formation, diabetes, rheumatoid arthritis, ischemia, neurodegenerative diseases and muscular dystrophies (David et al, 1993;Saito et al, 1993;Mouatt-Prigent et al, 1996;Hirsch et al, 1997;Ishikawa et al, 1999;Horikawa et al, 2000;Richard et al, 2000;Tidball and Spencer 2000;Tamada et al, 2001;Trumbeckaite et al, 2003). Moreover, calpains play pivotal roles in physiological and biological phenomena such as signal transduction, cell spreading and motility, apoptosis, regulation of cell cycle, and regulation of muscle cell differentiation (Huttenlocher et al, 1997;Potter et al, 1998;Villa et al, 1998;Atencio et al, 2000;Barnoy et al, 2000;Cottin et al, 2000;Patel and Lane, 2000;Dourdin et al, 2001;Glading et al, 2001;Sato and Kawashima, 2001).…”