Sarika Srivastava, Ph.D.
Affiliations: | 2005 | University of Miami, Coral Gables, FL |
Area:
Cell Biology, Molecular BiologyGoogle:
"Sarika Srivastava"Mean distance: 23.34
Parents
Sign in to add mentor| Carlos T. Moraes | grad student | 2005 | University of Miami | |
| (Natural and engineered strategies that modulate oxidative phosphorylation defects associated with mitochondrial DNA mutations.) | ||||
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Publications
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| Patel PA, Liang C, Arora A, et al. (2020) Haploinsufficiency of X-linked intellectual disability gene CASK induces post-transcriptional changes in synaptic and cellular metabolic pathways. Experimental Neurology. 113319 |
| McMillan RP, Stewart S, Budnick JA, et al. (2019) Quantitative Variation in m.3243A > G Mutation Produce Discrete Changes in Energy Metabolism. Scientific Reports. 9: 5752 |
| LaConte LEW, Chavan V, Elias AF, et al. (2018) Two microcephaly-associated novel missense mutations in CASK specifically disrupt the CASK-neurexin interaction. Human Genetics |
| Srivastava S. (2017) The Mitochondrial Basis of Aging and Age-Related Disorders. Genes. 8 |
| Chavan V, Willis J, Walker SK, et al. (2017) Correction: Central Presynaptic Terminals Are Enriched in ATP but the Majority Lack Mitochondria. Plos One. 12: e0181140 |
| Mukherjee K, Clark HR, Chavan V, et al. (2016) Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy. Journal of Visualized Experiments : Jove |
| Srivastava S. (2016) Emerging therapeutic roles for NAD(+) metabolism in mitochondrial and age-related disorders. Clinical and Translational Medicine. 5: 25 |
| Srivastava S, McMillan R, Willis J, et al. (2016) X-linked intellectual disability gene CASK regulates postnatal brain growth in a non-cell autonomous manner. Acta Neuropathologica Communications. 4: 30 |
| Chavan V, Willis J, Walker SK, et al. (2015) Central presynaptic terminals are enriched in ATP but the majority lack mitochondria. Plos One. 10: e0125185 |
| Srivastava S, Gonzalez Herrera KN, Proacccio V, et al. (2012) Low level of MtDNA mutation promotes mitochondrial bioenergetics and oxidative metabolism via retrograde signaling Mitochondrion. 12: 553 |