View Dr. Bayer's Publications on PubMed
Vest R. S., Davies K. D., O'Leary H., Port J. D., Bayer K. U. (2007) Dual mechanism of a natural CaMKII inhibitor. Mol Biol Cell., 18(12):5024-33.
O’Leary, H., Lasda, E. and Bayer, K. U. (2006) CaMKIIb association with the actin cytoskeleton is regulated by alternative splicing. Mol. Biol. Cell., 17:4646-4665.
Bayer, K. U., LeBel, E., McDonald, G. L., O’Leary, H., Schulman, H. and DeKoninck, P. (2006) Transition from reversible to persistant binding of CaMKII to postsynaptic sites and NR2B. J. Neurosci.. 26, 1164-1174.
Fink, C., Bayer, K. U., Myers, J. W., Ferrell, J. E. Schulman, H. and Meyer, T. (2003) Selective regulation of neurite extension, movement and branching by the b but not the a isoform of CaMKII. Neuron, 39, 283-297.
Bayer, K. U., De Koninck, P. and Schulman, H. (2002) Alternative splicing modulates the frequency-dependent response of CaMKII to Ca2+-oscillations. EMBO J., 21, 3590-3597.
Bayer, K.-U., De Koninck, P., Leonard, A.S., Hell, J.W. and Schulman, H. (2001) Interaction with the NMDA receptor locks CaMKII in an active conformation. Nature, 411, 801-805.
Bayer, K.-U., Harbers, K. and Schulman, H. (1998) aKAP is an anchoring protein for a novel CaM kinase II isoform in skeletal muscle. EMBO J., 17, 5598-5605.
Bayer, K.-U., Löhler, J. and Harbers, K. (1996) An alternative, nonkinase product of the brain-specifically expressed Ca2+/calmodulin-dependent kinase II a isoform gene in skeletal muscle. Mol. Cell. Biol., 16, 29-36.