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Melissa R. Regan

Researcher at Johns Hopkins University

Publications -  8
Citations -  2287

Melissa R. Regan is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Glutamate receptor & Transgene. The author has an hindex of 7, co-authored 8 publications receiving 2111 citations.

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β-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression

TL;DR: Using a blinded screen of 1,040 FDA-approved drugs and nutritionals, it is discovered that many β-lactam antibiotics are potent stimulators of GLT1 expression, and this action appears to be mediated through increased transcription of theGLT1 gene.
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Neuronal Exosomal miRNA-dependent Translational Regulation of Astroglial Glutamate Transporter GLT1

TL;DR: A new neuron-to-astrocyte communication pathway is characterized and miRNAs that modulate GLT1 protein expression in astrocytes in vitro and in vivo are identified.
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Variations in Promoter Activity Reveal a Differential Expression and Physiology of Glutamate Transporters by Glia in the Developing and Mature CNS

TL;DR: These studies of GLT-1 and GLAST promoter activity, protein expression, and glutamate uptake revealed a close correlation between transgenic reporter signals and uptake capacity, indicating that these mice provide the means to monitor the expression and regulation of glutamate transporters in situ.
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The type 1 inositol 1,4,5-trisphosphate receptor gene is altered in the opisthotonos mouse

TL;DR: The genetic and molecular data presented here demonstrate that the type 1 inositol 1,4,5-trisphosphate receptor (IP3R1) protein, which serves as an IP3-gated channel to release calcium from intracellular stores, is altered in the optmutant, suggesting that the convulsions and ataxia observed in opt mice may be caused by the physiological dysregulation of a functional IP3R 1 protein.
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Propentofylline-induced astrocyte modulation leads to alterations in glial glutamate promoter activation following spinal nerve transection.

TL;DR: The ability of propentofylline to alter glial glutamate transporters highlights the importance of controlling aberrant glial activation in neuropathic pain and suggests one possible mechanism for the anti-allodynic action of this drug.