Volume 94, Issue 6, Pages 1035-1037 (December 2018) Journal Club    Kidney International  Volume 94, Issue 6, Pages 1035-1037 (December 2018) DOI: 10.1016/j.kint.2018.10.006 Copyright © 2018 Terms and Conditions

Figure 1 Schematic model of the relationship between Ca2+/CaMK4 signaling and actin stability in podocytes. CAMK, Ca2+/calmodulin-dependent protein kinase; LPS, lipopolysaccharide; P, phosphate; Rac1, Ras-related C3 botulinum toxin substrate 1; TLR, toll-like receptor; TRPC5, transient receptor potential channel 5. Reprinted with permission from Maeda K, Otomo K, Yoshida N, et al. CaMK4 compromises podocyte function in autoimmune and nonautoimmune kidney disease. J Clin Invest. 2018;128:3445–3459; https://doi.org/10.1172/JCI99507. Copyright © 2018 American Society for Clinical Investigation. Kidney International 2018 94, 1035-1037DOI: (10.1016/j.kint.2018.10.006) Copyright © 2018 Terms and Conditions