Abstract
Tyrosine nitration results in altered function of selective proteins, including human smooth muscle L-type calcium channel, hCa(v)1.2b. We report here that Ca(v)1.2 is also subject to "denitration". Cell lysates from activated macrophage-like cell line, RAW264.7 cells, reversed peroxynitrite-induced nitration of the carboxy terminus of Ca(v)1.2 in a 1D gel assay. Tyrosine phosphorylation of the calcium channel by c-src kinase was blocked by nitration but reversed by pretreatment with RAW264.7 cell lysates. These findings indicate that denitration may be a physiological mechanism to restore cellular excitability during inflammation.