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Abstract
RGS10 plays an important role in regulating microglia activation; however, the mechanism of RGS10 is poorly understood. RGS10 has the unique ability to translocate to the nucleus upon PKA phosphorylation. Inflammatory cytokine production is increased upon loss of RGS10, suggesting that RGS10 plays an important anti-inflammatory role. Additionally, literature suggests RGS10 augments anti-inflammatory CREB signaling via interactions with PKA. When stimulated by PKA, CREB binds to the CRE consensus sequence on the promoters of inflammatory cytokines. First, we hypothesize that RGS10 is indirectly associating with chromatin or in a complex with other DNA binding proteins at the promoters of inflammatory cytokines. Secondly, we hypothesize that the PKA phosphorylation site on RGS10 is critical to its regulatory activity within the nucleus.