Loss of the batten disease protein CLN3 leads to mis-trafficking of M6PR and defective autophagic-lysosomal reformation.

MLA

Calcagni’, Alessia, et al. “Loss of the Batten Disease Protein CLN3 Leads to Mis-Trafficking of M6PR and Defective Autophagic-Lysosomal Reformation.” Nature Communications, vol. 14, no. 1, July 2023, p. 3911. EBSCOhost, https://doi.org/10.1038/s41467-023-39643-7.

APA

Calcagni’, A., Staiano, L., Zampelli, N., Minopoli, N., Herz, N. J., Di Tullio, G., Huynh, T., Monfregola, J., Esposito, A., Cirillo, C., Bajic, A., Zahabiyon, M., Curnock, R., Polishchuk, E., Parkitny, L., Medina, D. L., Pastore, N., Cullen, P. J., Parenti, G., … Ballabio, A. (2023). Loss of the batten disease protein CLN3 leads to mis-trafficking of M6PR and defective autophagic-lysosomal reformation. Nature Communications, 14(1), 3911. https://doi.org/10.1038/s41467-023-39643-7

Chicago

Calcagni’, Alessia, Leopoldo Staiano, Nicolina Zampelli, Nadia Minopoli, Niculin J Herz, Giuseppe Di Tullio, Tuong Huynh, et al. 2023. “Loss of the Batten Disease Protein CLN3 Leads to Mis-Trafficking of M6PR and Defective Autophagic-Lysosomal Reformation.” Nature Communications 14 (1): 3911. doi:10.1038/s41467-023-39643-7.