Author:
Mandya Aishwarya S,Cheramangalam Rajit Narayanan,Jaiswal Manish
Reference231 articles.
1. Abeliovich, A., & Gitler, A. D. (2016, November 10). Defects in trafficking bridge Parkinson’s disease pathology and genetics. Nature, 539(7628), 207–216.
2. Aperia, A. (2007, Jan). New roles for an old enzyme: Na,K-ATPase emerges as an interesting drug target. Journal of Internal Medicine, 261(1), 44–52.
3. Ashmore, L. J., Hrizo, S. L., Paul, S. M., Van Voorhies, W. A., Beitel, G. J., & Palladino, M. J. (2009, September). Novel mutations affecting the Na, K ATPase alpha model complex neurological diseases and implicate the sodium pump in increased longevity. Human Genetics, 126(3), 431–447.
4. Auluck, P. K., Chan, H. Y. E., Trojanowski, J. Q., Lee, V. M. Y., & Bonini, N. M. (2002, February 1). Chaperone suppression of alpha-synuclein toxicity in a Drosophila model for Parkinson’s disease. Science, 295(5556), 865–868.
5. Baldwin, K. R., Godena, V. K., Hewitt, V. L., & Whitworth, A. J. (2016, June 15). Axonal transport defects are a common phenotype in Drosophila models of ALS. Human Molecular Genetics, 25(12), 2378–2392.
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献