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Given the aforementioned findings from D2-like receptors, we sought in this study to determine the molecular mechanisms involved in GPCR desensitization that could differ from the conventionally accepted mechanism: uncoupling

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( A ) Under IL-13stimulated conditions, ALOX15 (15LO1) knockdown (KD) increases intracellular GSH and the GSH:GSSG ratio toward control conditions ( n = 6)

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FAK-paxillin (focal adhesion kinasepaxillin): Involved in cell adhesion, migration, and signaling