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1 Cho, D.H., Kim, J.K., and Jo, E.K. (2020). Mitophagy and innate immunity in infection. Mol. Cells 43, 10-22./   DOI View Article
2 Kwon, C., Lee, J.H., and Yun, H.S. (2020a). SNAREs in plant biotic and abiotic stress responses. Mol. Cells 43, 501-508./   DOI View Article
3 Choi, J.W., Kim, J.W., Nguyen, L.P., Nguyen, H.C., Park, E.M., Choi, D.H., Han, K.M., Kang, S.M., Tark, D., Lim, Y.S., et al. (2020). Nonstructural NS5A protein regulates LIM and SH3 domain protein 1 to promote hepatitis C virus propagation. Mol. Cells 43, 469-478./   DOI View Article
4 Chung, K.W., Kim, J.S., and Lee, K.S. (2020). A database of Caenorhabditis elegans locomotion and body posture phenotypes for the peripheral neuropathy model. Mol. Cells 43, 880-888./   DOI View Article
5 Jeong, S., Ahn, J., Kwon, A.R., and Ha, N.C. (2020). Cleavage-dependent activation of ATP-dependent protease HslUV from Staphylococcus aureus. Mol. Cells 43, 694-704./   DOI View Article
6 Ahmed, M.B., Islam, S.U., Sonn, J.K., and Lee, Y.S. (2020). PRP4 kinase domain loss nullifies drug resistance and epithelial-mesenchymal transition in human colorectal carcinoma cells. Mol. Cells 43, 662-670./   DOI View Article
7 Nguyen, L.P., Nguyen, H.T., Yong, H.J., Reyes-Alcaraz, A., Lee, Y.N., Park, H.K., Na, Y.H., Lee, C.S., Ham, B.J., Seong, J.Y., et al. (2020). Establishment of a NanoBiT-based cytosolic Ca(2+) sensor by optimizing calmodulinbinding motif and protein expression levels. Mol. Cells 43, 909-920./   DOI View Article
8 Lee, B., Park, S.J., Lee, S., Park, S.E., Lee, E., Song, J.J., Byun, Y., and Kim, S. (2020a). Identification of the antidepressant vilazodone as an inhibitor of inositol polyphosphate multikinase by structure-based drug repositioning. Mol. Cells 43, 222-227./   DOI View Article
9 Jang, K.H., Hwang, Y., and Kim, E. (2020). PARP1 impedes SIRT1-mediated autophagy during degeneration of the retinal pigment epithelium under oxidative stress. Mol. Cells 43, 632-644./   DOI View Article
10 Choi, E.J., Jeon, C.H., Park, D.H., and Kwon, T.H. (2020). Allithiamine exerts therapeutic effects on sepsis by modulating metabolic flux during dendritic cell activation. Mol. Cells 43, 964-973./   DOI View Article