| First Author | Xie Z | Year | 2008 |
| Journal | Mol Cell | Volume | 31 |
| Issue | 5 | Pages | 660-70 |
| PubMed ID | 18775326 | Mgi Jnum | J:138772 |
| Mgi Id | MGI:3806381 | Doi | 10.1016/j.molcel.2008.06.024 |
| Citation | Xie Z, et al. (2008) RGS13 acts as a nuclear repressor of CREB. Mol Cell 31(5):660-70 |
| abstractText | Cyclic AMP-induced phosphorylation of the transcription factor CREB elicits expression of genes mediating diverse biological functions. In lymphoid organs, the neurotransmitter norepinephrine stimulates beta(2)-adrenergic receptors on B lymphocytes to promote CREB-dependent expression of genes like the B cell Oct 2 coactivator (OCA-B). Although CREB phosphorylation recruits cofactors such as CBP/p300 to stimulate transcription, bona fide endogenous inhibitors of CREB-coactivator or CREB-DNA interactions have not emerged. Here, we identified RGS13, a member of the Regulator of G protein Signaling (RGS) protein family, as a nuclear factor that suppresses CREB-mediated gene expression. cAMP or Ca(2+) signaling promoted RGS13 accumulation in the nucleus, where it formed a complex with phosphorylated CREB and CBP/p300. RGS13 reduced the apparent affinity of pCREB for both the CRE and CBP. B lymphocytes from Rgs13(-/-) mice had more beta(2)-agonist-induced OCA-B expression. Thus, RGS13 inhibits CREB-dependent transcription of target genes through disruption of complexes formed at the promoter. |
