| Year |
Citation |
Score |
| 2010 |
Cao S, Hewett JW, Yokoi F, Lu J, Buckley AC, Burdette AJ, Chen P, Nery FC, Li Y, Breakefield XO, Caldwell GA, Caldwell KA. Chemical enhancement of torsinA function in cell and animal models of torsion dystonia. Disease Models & Mechanisms. 3: 386-96. PMID 20223934 DOI: 10.1242/Dmm.003715 |
0.598 |
|
| 2010 |
Su LJ, Auluck PK, Outeiro TF, Yeger-Lotem E, Kritzer JA, Tardiff DF, Strathearn KE, Liu F, Cao S, Hamamichi S, Hill KJ, Caldwell KA, Bell GW, Fraenkel E, Cooper AA, et al. Compounds from an unbiased chemical screen reverse both ER-to-Golgi trafficking defects and mitochondrial dysfunction in Parkinson's disease models. Disease Models & Mechanisms. 3: 194-208. PMID 20038714 DOI: 10.1242/Dmm.004267 |
0.663 |
|
| 2008 |
Hamamichi S, Rivas RN, Knight AL, Cao S, Caldwell KA, Caldwell GA. Hypothesis-based RNAi screening identifies neuroprotective genes in a Parkinson's disease model. Proceedings of the National Academy of Sciences of the United States of America. 105: 728-33. PMID 18182484 DOI: 10.1073/Pnas.0711018105 |
0.675 |
|
| 2006 |
Dickey CA, Yue M, Lin WL, Dickson DW, Dunmore JH, Lee WC, Zehr C, West G, Cao S, Clark AM, Caldwell GA, Caldwell KA, Eckman C, Patterson C, Hutton M, et al. Deletion of the ubiquitin ligase CHIP leads to the accumulation, but not the aggregation, of both endogenous phospho- and caspase-3-cleaved tau species. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 26: 6985-96. PMID 16807328 DOI: 10.1523/Jneurosci.0746-06.2006 |
0.513 |
|
| 2006 |
Cooper AA, Gitler AD, Cashikar A, Haynes CM, Hill KJ, Bhullar B, Liu K, Xu K, Strathearn KE, Liu F, Cao S, Caldwell KA, Caldwell GA, Marsischky G, Kolodner RD, et al. Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models. Science (New York, N.Y.). 313: 324-8. PMID 16794039 DOI: 10.1126/Science.1129462 |
0.641 |
|
| 2005 |
Cao S, Gelwix CC, Caldwell KA, Caldwell GA. Torsin-mediated protection from cellular stress in the dopaminergic neurons of Caenorhabditis elegans. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 25: 3801-12. PMID 15829632 DOI: 10.1523/Jneurosci.5157-04.2005 |
0.607 |
|
| 2005 |
Caldwell GA, Cao S, Izevbaye I, Caldwell KA. Use of C. elegans to model human movement disorders Movement Disorders. 111-126. DOI: 10.1016/B978-012088382-0/50009-8 |
0.442 |
|
| 2004 |
Caldwell GA, Cao S, Gelwix CC, Sexton EG, Caldwell KA. An animal model to discern torsin function: suppression of protein aggregation in C. elegans. Advances in Neurology. 94: 79-85. PMID 14509658 |
0.483 |
|
| 2003 |
Caldwell GA, Cao S, Sexton EG, Gelwix CC, Bevel JP, Caldwell KA. Suppression of polyglutamine-induced protein aggregation in Caenorhabditis elegans by torsin proteins. Human Molecular Genetics. 12: 307-19. PMID 12554684 DOI: 10.1093/Hmg/Ddg027 |
0.567 |
|
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