Cite
Amyloidogenic 60–71 deletion/ValThr insertion mutation of apolipoprotein A-I generates a new aggregation-prone segment that promotes nucleation through entropic effects.
MLA
Namba, Norihiro, et al. “Amyloidogenic 60–71 Deletion/ValThr Insertion Mutation of Apolipoprotein A-I Generates a New Aggregation-Prone Segment That Promotes Nucleation through Entropic Effects.” Scientific Reports, vol. 13, no. 1, Oct. 2023, pp. 1–13. EBSCOhost, https://doi.org/10.1038/s41598-023-45803-y.
APA
Namba, N., Ohgita, T., Tamagaki-Asahina, H., Nishitsuji, K., Shimanouchi, T., Sato, T., & Saito, H. (2023). Amyloidogenic 60–71 deletion/ValThr insertion mutation of apolipoprotein A-I generates a new aggregation-prone segment that promotes nucleation through entropic effects. Scientific Reports, 13(1), 1–13. https://doi.org/10.1038/s41598-023-45803-y
Chicago
Namba, Norihiro, Takashi Ohgita, Hiroko Tamagaki-Asahina, Kazuchika Nishitsuji, Toshinori Shimanouchi, Takeshi Sato, and Hiroyuki Saito. 2023. “Amyloidogenic 60–71 Deletion/ValThr Insertion Mutation of Apolipoprotein A-I Generates a New Aggregation-Prone Segment That Promotes Nucleation through Entropic Effects.” Scientific Reports 13 (1): 1–13. doi:10.1038/s41598-023-45803-y.