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Calcineurin and glial signaling: Neuroinflammation and beyond
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نویسنده
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furman j.l. ,norris c.m.
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منبع
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journal of neuroinflammation - 2014 - دوره : 11 - شماره : 0
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چکیده
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Similar to peripheral immune/inflammatory cells,neuroglial cells appear to rely on calcineurin (cn) signaling pathways to regulate cytokine production and cellular activation. several studies suggest that harmful immune/inflammatory responses may be the most impactful consequence of aberrant cn activity in glial cells. however,newly identified roles for cn in glutamate uptake,gap junction regulation,ca2+ dyshomeostasis,and amyloid production suggest that cn's influence in glia may extend well beyond neuroinflammation. the following review will discuss the various actions of cn in glial cells,with particular emphasis on astrocytes,and consider the implications for neurologic dysfunction arising with aging,injury,and/or neurodegenerative disease. © 2014 furman and norris; licensee biomed central ltd.
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کلیدواژه
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Alzheimer's disease; Amyloid; Astrocytes; Ca2+ regulation; Calcineurin; Gap junction; Glutamate; Neurodegeneration; Neuroinflammation
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آدرس
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department of neurology,school of medicine,washington university,660 south euclid,st. louis,mo 63110, United States, pharmacology and nutritional sciences and the sanders-brown center on aging,university of kentucky college of medicine,800 south limestone st.,lexington,ky 40536, United States
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Authors
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