CALHM1 and its polymorphism P86L differentially control Ca²⁺homeostasis, mitogen-activated protein kinase signaling, and cell vulnerability upon exposure to amyloid β.

MLA

Moreno-Ortega, Ana José, et al. “CALHM1 and Its Polymorphism P86L Differentially Control Ca²⁺homeostasis, Mitogen-Activated Protein Kinase Signaling, and Cell Vulnerability upon Exposure to Amyloid β.” Aging Cell, vol. 14, no. 6, Dec. 2015, pp. 1094–102. EBSCOhost, https://doi.org/10.1111/acel.12403.

APA

Moreno-Ortega, A. J., Buendia, I., Mouhid, L., Egea, J., Lucea, S., Ruiz-Nuño, A., López, M. G., & Cano-Abad, M. F. (2015). CALHM1 and its polymorphism P86L differentially control Ca²⁺homeostasis, mitogen-activated protein kinase signaling, and cell vulnerability upon exposure to amyloid β. Aging Cell, 14(6), 1094–1102. https://doi.org/10.1111/acel.12403

Chicago

Moreno-Ortega, Ana José, Izaskun Buendia, Lamia Mouhid, Javier Egea, Susana Lucea, Ana Ruiz-Nuño, Manuela G López, and María F Cano-Abad. 2015. “CALHM1 and Its Polymorphism P86L Differentially Control Ca²⁺homeostasis, Mitogen-Activated Protein Kinase Signaling, and Cell Vulnerability upon Exposure to Amyloid β.” Aging Cell 14 (6): 1094–1102. doi:10.1111/acel.12403.