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GPS2 encodes a protein involved in G protein-mitogen-activated protein kinase (MAPK) signaling cascades.
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The study of adipose tissue from humans with and without obesity revealed correlations between reduced GPS2 expression in macrophages, elevated systemic and adipose tissue inflammation, and diabetic status.
our studies identify GPS2 functions as a tumor suppressor in LPS (show IRF6 Proteins) and its downregulation is correlated to prognosis of LPS (show IRF6 Proteins).
Posttranslational modification of GPS2 by SUMOylation may serve as a key factor that regulates the function of GPS2 in vivo.
regulation of GPS2 by posttranslational modifications provides an effective strategy for modulating its molecular function within the nuclear compartment.
Chromosomal translocation in a pediatric undifferentiated spindle cell sarcoma have characterized this alteration to show rearrangement of the MLL4 and GPS2 genes, resulting in fusion gene MLL4-GPS2, the expression of which promotes independent growth.
GPS2 is required for the association of viral NS5A with VAP-A (show VAPA Proteins) and hepatitis C virus replication.
expression of the transcriptional corepressor complex subunits GPS2 and SMRT was significantly reduced in obese adipose tissue, inversely correlated to inflammatory status
Results show for the first time that GPS-2 is differentially methylated at a site that lacks known methylation motifs and that the methylation state is detected by the immune system
metabolically important coregulator GPS2 functions as a hitherto unrecognized transrepression mediator of interactions between SUMOylated nuclear receptors and the N-CoR (show NCOR1 Proteins) corepressor complex
Results show that the N-CoR (show NCOR1 Proteins)-HDAC3 (show HDAC3 Proteins) complex inhibits JNK (show MAPK8 Proteins) activation through the associated GPS2 subunit and thus could potentially provide an alternative mechanism for hormone-mediated antagonism of AP-1 (show FOSB Proteins) function.
In macrophage-specific Gps2-knockout mice, inappropriate co-repressor complex function caused enhancer activation, pro-inflammatory gene expression and hypersensitivity toward metabolic-stress signals. By contrast, transplantation of GPS2-overexpressing bone marrow into two mouse models of obesity (ob/ob and diet-induced obesity) reduced inflammation and improved insulin (show INS Proteins) sensitivity.
GPS2 is required for restricting the activation of TLR and BCR (show BCR Proteins) signaling pathways and the AKT (show AKT1 Proteins)/FOXO1 (show FOXO1 Proteins) pathway in immune cells based on direct inhibition of Ubc13 (show UBE2N Proteins) enzymatic activity
GPS2 stabilizes KDM4A (show KDM4A Proteins) on target promoters by inhibiting Ubc13 (show UBE2N Proteins)/RNF8 (show RNF8 Proteins) ubiquitination.
GPS2 binds to active PPARgamma (show PPARG Proteins), facilitates its repression by NCoR (show NCOR1 Proteins), and is required for the optimal NCoR (show NCOR1 Proteins) corepressor function for PPARgamma (show PPARG Proteins).
GPS2 as a molecular guardian required for precise control of inflammatory responses involved in immunity and homeostasis.
This gene encodes a protein involved in G protein-mitogen-activated protein kinase (MAPK) signaling cascades. When overexpressed in mammalian cells, this gene could potently suppress a RAS- and MAPK-mediated signal and interfere with JNK activity, suggesting that the function of this gene may be signal repression. The encoded protein is an integral subunit of the NCOR1-HDAC3 (nuclear receptor corepressor 1-histone deacetylase 3) complex, and it was shown that the complex inhibits JNK activation through this subunit and thus could potentially provide an alternative mechanism for hormone-mediated antagonism of AP1 (activator protein 1) function.
G protein pathway suppressor 2
, G-protein pathway suppressor 2