Bridget Shafit-Zagardo

Yeshiva University, New York, NY, United States 
Pathology, Neuroscience Biology
"Bridget Shafit-Zagardo"
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Robert J. Desnick grad student (Cell Biology Tree)
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Shafit-Zagardo B, Sidoli S, Goldman JE, et al. (2023) TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury. Cells. 12
DuBois JC, Ray AK, Gruber RC, et al. (2019) Akt3-Mediated Protection Against Inflammatory Demyelinating Disease. Frontiers in Immunology. 10: 1738
Mocholi E, Dowling SD, Botbol Y, et al. (2018) Autophagy Is a Tolerance-Avoidance Mechanism that Modulates TCR-Mediated Signaling and Cell Metabolism to Prevent Induction of T Cell Anergy. Cell Reports. 24: 1136-1150
Shafit-Zagardo B, Gruber RC, DuBois JC. (2018) The Role of TAM Family Receptors and Ligands in the Nervous System: From Development to Pathobiology. Pharmacology & Therapeutics
Ray AK, DuBois JC, Gruber RC, et al. (2017) Loss of Gas6 and Axl signaling results in extensive axonal damage, motor deficits, prolonged neuroinflammation, and less remyelination following cuprizone exposure. Glia
Gruber RC, LaRocca D, Minchenberg SB, et al. (2015) The control of reactive oxygen species production by SHP-1 in oligodendrocytes. Glia
Gruber RC, Ray AK, Johndrow CT, et al. (2014) Targeted GAS6 delivery to the CNS protects axons from damage during experimental autoimmune encephalomyelitis. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 34: 16320-35
O'Guin KN, Gruber RC, Raine CS, et al. (2014) Gas6 enhances axonal ensheathment by MBP+ membranous processes in human DRG/OL promyelinating co-cultures. Asn Neuro. 6: e00135
Tsiperson V, Gruber RC, Goldberg MF, et al. (2013) Suppression of inflammatory responses during myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis is regulated by AKT3 signaling. Journal of Immunology (Baltimore, Md. : 1950). 190: 1528-39
Weinger JG, Davies P, Acker CM, et al. (2012) Mice devoid of Tau have increased susceptibility to neuronal damage in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis. Journal of Neuropathology and Experimental Neurology. 71: 422-33
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