RETRACTED: L-Type Ca2+ Channel Facilitation Mediated by Phosphorylation of the β Subunit by CaMKII

By Chad E. Grueter, S. Abiria, I. Dzhura, Yuejin Wu, A. Ham, P. Mohler, M. Anderson, R. Colbran. 2006

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Cell Biology of Ischemia/Reperfusion Injury (2012, background): “CaMK-II can phosphorylate and activate L-type Ca2þ channels (Grueter et al., 2006) and Naþ channels (Wagner et al., 2006), both of which would be expected to further exacerbate the large increases in intracellular Ca2þ associated with I/R.”
A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation. (2008, background): “The multifunctional calcium/calmodulin (Ca2+/CaM)-dependent protein kinase II (CaMKII) couples increases in Ca2+ to activation of ion channels (Grueter et al., 2006), gene transcription (Backs et al., 2006), and apoptosis (Zhu et al., 2003; Yang et al., 462 Cell 133, 462–474, May 2, 2008 ª2008…”
Calcium cycling and signaling in cardiac myocytes. (2008, background): “α1C itself and the accessory β2 subunit have been implicated in mediating ICa facilitation (18, 19).”