近期论文

查看导师新发文章 （温馨提示：请注意重名现象，建议点开原文通过作者单位确认）

M'Angale, P.G., and B.E. Staveley, 2017. A loss-of-function Pdxk model of Parkinson Disease in Drosophila can be suppressed by Buffy. BioMed Central Research Notes 10: 205. DOI: 10.1186/s13104-017-2526-8 (9 pages). M'Angale, P.G., and B.E. Staveley, 2017. Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila. Genome 60(3): 241-247. DOI: 10.1139/gen-2016-0165. Epub as “Just-IN” December 22, 2016. M'Angale, P.G., and B.E. Staveley, 2017. Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease. PeerJ 5:e2974. DOI: 10.7717/peerj.2974 (19 pages). M'Angale, P.G., and B.E. Staveley, 2017. Inhibition of Mitochondrial Calcium Uptake 1 in Drosophila neurons. Genetics and Molecular Research 16(1): gmr16019436. DOI: 10.4238/gmr156019436 (11 pages). Merzetti, E.M., L.A. Dolomount, and B.E. Staveley, 2017. The FBXO7 homologue nutcracker and binding partner PI31 in Drosophila melanogaster models of Parkinson Disease. Genome 60(1): 46-54. DOI: 10.1139/gen-2016-0087. Epub as “Just-IN” September 15, 2016. M'Angale, P.G., and B.E. Staveley, 2017. The HtrA2 Drosophila model of Parkinson Disease is suppressed by the pro-survival Bcl-2 Buffy. Genome 60(1): 1-7. DOI: 10.1139/gen-2016-0069. Epub as “Just-IN” August 30, 2016. M'Angale, P.G., and B.E. Staveley, 2016. Co-expression of Buffy with Buffy-RNAi produces an intermediate phenotype in the Drosophila eye. Drosophila Information Services 99: 14-16. M'Angale, P.G., and B.E. Staveley, 2016. Inhibition of the Lifeguard homologue CG3814 in Drosophila melanogaster. Genetics and Molecular Research 15(4): gmr15049290.DOI: 10.4238/gmr15049290 (11 pages). M'Angale, P.G., and B.E. Staveley, 2016. The inhibition of CG2076, the GHITM homologue in neurons of Drosophila melanogaster can be rescued by Buffy. Journal of RNAi and Gene Silencing 12: 521-527. M'Angale, P.G., and B.E. Staveley, 2016. A loss of porin model of Parkinson disease in Drosophila is suppressed by Buffy. Journal of Biomedical Science 23: 84. DOI: 10.1186/s12929-016-0300-1 (9 pages). Merzetti, E.M., and B.E. Staveley, 2016. Identification of potential PARIS homologs in Drosophila melanogaster. Genetics and Molecular Research 15(4): DOI: gmr15048934. DOI: 10.4238/gmr15048934 (12 pages). M'Angale, P.G., and B.E. Staveley, 2016. Inhibition of autophagy genes, Atg6 and Pi3K59F, in Drosophila models of Parkinson Disease. Genetics and Molecular Research 15(4): gmr15048953. DOI: 10.4238/gmr15048953 (13 pages). M'Angale, P.G., and B.E. Staveley, 2016. Bcl-2 homologue Debcl enhances α-synuclein-induced phenotypes in Drosophila. PeerJ 4: e2461. DOI: 10.7717/peerj.2461 (17 pages). Merzetti, E.M., and B.E. Staveley, 2016. Altered expression of CG5961, a putative Drosophila melanogaster homologue of FBXO9, provides a new model of Parkinson disease. Genetics and Molecular Research 15(2): gmr.15028579. DOI: 10.4238/gmr.15028579 (10 pages). M'Angale, P.G., and B.E. Staveley, 2016. The Bcl-2 homologue Buffy rescues α-synuclein-induced Parkinson disease-like phenotypes in Drosophila. BioMed Central Neuroscience 17(1):24. DOI: 10.1186/s12868-016-0261-z (8 pages). Slade, J.D., and B.E. Staveley, 2016. Extended longevity and survivorship during amino-acid starvation in a Drosophila Sir2 mutant heterozygote. Genome 57(5): 311-318. DOI: 10.1139/gen-2015-0213. Slade, J.D., and B.E. Staveley, 2016. Manipulation of components that control feeding behavior in Drosophila melanogaster increases sensitivity to amino-acid starvation. Genetics and Molecular Research 15 (1): gmr.15017489. DOI: 10.4238/gmr.15017489 (12 pages). Slade, J.D., and B.E. Staveley, 2016. Enhanced survival of Drosophila Akt1 hypomorphs during amino-acid starvation requires foxo. Genome 57(2): 87-93. DOI: 10.1139/gen-2015-0113. Epub November 20, 2015. Chavoshi, M.A., and B.E. Staveley, 2016. Inhibition of foxo and minibrain in dopaminergic neurons can model aspects of Parkinson Disease in Drosophila melanogaster. Advances in Parkinson’s Disease 5(1): 1-6. DOI: 10.4236/apd.2015.51001. Merzetti, E.M., and B.E. Staveley, 2015. spargel, the PGC-1α homologue, in models of Parkinson Disease in Drosophila melanogaster. BioMed Central Neuroscience 16: 70 (8 pages). DOI: 10.1186/s12868-015-0210-2. Slade, F.A., and B.E. Staveley, 2015. arm-Gal4 inheritance influences development and lifespan in Drosophila melanogaster. Genetics and Molecular Research 14(4): 12788-12796. DOI: 10.4238/2015.October.19.22. Todd, A.M., and B.E. Staveley, 2015. Pink1 rescues Gal4-induced developmental defects in the drosophila eye. Advances in Parkinson's Disease 4(3): 43-48. DOI: 10.4236/apd.2015.43006. Slade, J.D., and B.E. Staveley, 2015. Compensatory growth in Drosophila Akt1 mutants. BioMed Central Research Notes 8: 77. DOI: 10.1186/s13104-015-1032-0 (10 pages). Staveley B.E., 2015. Drosophila Models of Parkinson Disease. In Movement Disorders: Genetics and Models, Second Edition, Elsevier Inc. Mark S. LeDoux (Ed.) (invited book chapter, 345-354). Sheaves, D.W., and B.E. Staveley, 2014. A novel GMR-Gal4 insertion produces a rough eye phenotype. Drosophila Information Services 97: 141-143.