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Marge Williams

Researcher at University of Pennsylvania

Publications -  4
Citations -  112

Marge Williams is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Receptor & Cell culture. The author has an hindex of 4, co-authored 4 publications receiving 107 citations.

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Interleukin‐1β stimulates macrophage inflammatory protein‐1α and ‐1β expression in human neuronal cells (NT2‐N)

TL;DR: Investigation of the mechanism(s) responsible for IL‐1β‐induced MIP‐1α and ‐1β expression demonstrated that IL-1β activated nuclear factor kappa B (NF‐κB) promoter‐directed luciferase activity in NT2‐N cells, suggesting that NF‐κBs is at least partially involved in the IL‐ 1β‐mediated action on MIP-1 α and ‬1β inNT2‐ N cells.
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A non‐peptide substance P antagonist (CP‐96,345) inhibits morphine‐induced NF‐κB promoter activation in human NT2‐N neurons

TL;DR: Investigation of the mechanism responsible for morphine‐induced activation of NF‐κB promoter in NT2‐N neurons demonstrated that morphine activates the SP promoter and induces SP expression in these cells, suggesting that morphine, by activating MOR, engages a positive feedback loop between NK‐1R and SP.
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Human central nervous system primitive neuroectodermal tumor expressing nerve growth factor receptors: CHP707m.

TL;DR: Although CHP707m is the first central nervous system PNET cell line proven to express NGF receptors, immunohistological survey of tissue sections prepared from human central nervous System PNETs showed that 13 of 35 contained NGF receptor‐positive tumor cells, suggesting more than one‐third of such tumors might be responsive to the effects of NGF.
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Human neuronal cells (NT2-N) express functional substance P and neurokinin-1 receptor coupled to MIP-1β expression

TL;DR: It is demonstrated that SP and NK‐1R presented in NT2‐N cells are functionally involved in the regulation of macrophage inflammatory protein 1 beta (MIP‐1β), an important β‐chemokine participating in the activation and directional migration of immune cells to sites of central nervous systems (CNS) inflammation.