Mahua Maulik, Ph.D.
Affiliations: | 2013 | Neuroscience | University of Alberta, Edmonton, Alberta, Canada |
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"Mahua Maulik"Mean distance: 53433
Parents
Sign in to add mentor| Satyabrata Kar | grad student | 2013 | University of Alberta | |
| (Cholesterol and Alzheimer's Disease-Related Pathology.) | ||||
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Publications
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| Maulik M, Vasan L, Bose A, et al. (2020) Amyloid-β regulates gap junction protein Connexin 43 trafficking in cultured primary astrocytes. The Journal of Biological Chemistry |
| Chung J, Phukan G, Vergote D, et al. (2018) Endosomal-lysosomal Cholesterol Sequestration by U18666A Differentially Regulates APP Metabolism in Normal and APP Overexpressing Cells. Molecular and Cellular Biology |
| Maulik M, Vergote D, Phukan G, et al. (2017) The Effects of Extracellular Serum Concentration on APP Processing in Npc1-Deficient APP-Overexpressing N2a Cells. Molecular Neurobiology |
| Maulik M, Peake K, Chung J, et al. (2015) APP overexpression in absence of NPC1 exacerbates metabolism of amyloidogenic proteins of Alzheimer's disease. Human Molecular Genetics |
| Banerjee M, Sasse VA, Wang Y, et al. (2015) Increased levels and activity of cathepsins B and D in kainate-induced toxicity. Neuroscience. 284: 360-73 |
| Maulik M, Thinakaran G, Kar S. (2013) Alterations in gene expression in mutant amyloid precursor protein transgenic mice lacking Niemann-Pick type C1 protein. Plos One. 8: e54605 |
| Maulik M, Westaway D, Jhamandas JH, et al. (2013) Role of cholesterol in APP metabolism and its significance in Alzheimer's disease pathogenesis. Molecular Neurobiology. 47: 37-63 |
| Maulik M, Ghoshal B, Kim J, et al. (2012) Mutant human APP exacerbates pathology in a mouse model of NPC and its reversal by a β-cyclodextrin. Human Molecular Genetics. 21: 4857-75 |
| Kodam A, Maulik M, Peake K, et al. (2010) Altered levels and distribution of amyloid precursor protein and its processing enzymes in Niemann-Pick type C1-deficient mouse brains. Glia. 58: 1267-81 |
| Gupta A, Maulik M, Nasipuri P, et al. (2007) Molecular diagnosis of Wilson disease using prevalent mutations and informative single-nucleotide polymorphism markers. Clinical Chemistry. 53: 1601-8 |