RGS8

Last update 08 May 2025

Basic Info

Synonyms

MGC119067, MGC119068, MGC119069

+ [4]

Introduction

Regulates G protein-coupled receptor signaling cascades, including signaling via muscarinic acetylcholine receptor CHRM2 and dopamine receptor DRD2 (By similarity). Inhibits signal transduction by increasing the GTPase activity of G protein alpha subunits, thereby driving them into their inactive GDP-bound form (PubMed:18434541). Modulates the activity of potassium channels that are activated in response to DRD2 and CHRM2 signaling (By similarity).

100 Clinical Results associated with RGS8

100 Translational Medicine associated with RGS8

0 Patents (Medical) associated with RGS8

Literatures (Medical) associated with RGS8

01 Oct 2024·Journal of Neurology

Anti-RGS8 paraneoplastic cerebellar ataxia is preferentially associated with a particular subtype of Hodgkin’s lymphoma

Article

Author: Desestret, Virginie ; Scharf, Madeleine ; Zorn, Kelsey C. ; Pleasure, Samuel J. ; Antoine, Jean-Christophe ; DeRisi, Joseph L. ; Wilson, Michael R ; Gelfand, Jeffrey M. ; Gelfand, Jeffrey M ; Do, Le-Duy ; Peter, Elise ; Rogemond, Véronique ; Tranchant, Christine ; Farina, Antonio ; DeRisi, Joseph L ; Pleasure, Samuel J ; Miske, Ramona ; Bartley, Christopher M ; Wilson, Michael R. ; Ngo, Thomas ; Ciano-Petersen, Nicolas Lundahl ; Pluvinage, John ; Dubois, Valérie ; Zorn, Kelsey C ; Perrot, Jimmy ; Bartley, Christopher M. ; Villagrán-García, Macarena ; Honnorat, Jérôme ; Traverse-Glehen, Alexandra

AbstractAtaxia with anti-regulator of G-protein signaling 8 autoantibodies (RGS8-Abs) is an autoimmune disease recently described in four patients. The present study aimed to identify other patients with RGS8-Abs, describe their clinical features, including the link between RGS8-related autoimmune cerebellar ataxia (ACA) and cancer. Patients with RGS8-Abs were identified retrospectively in the biological collections of the French Reference Center for Paraneoplastic Neurological Syndrome and the University of California San Francisco Center for Encephalitis and Meningitis. Clinical data were collected, and cerebrospinal fluid, serum, and tumor pathological samples were retrieved to characterize the autoantibodies and the associated malignancies. Only three patients with RGS8-Abs were identified. All of them presented with a pure cerebellar ataxia of mild to severe course, unresponsive to current immunotherapy regimens for ACA. Two patients presented with a Hodgkin lymphoma of the rare specific subtype called nodular lymphocyte-predominant Hodgkin lymphoma, with very mild extension. Autoantibodies detected in all patients enriched the same epitope on the RGS8 protein, which is an intracellular protein physiologically expressed in Purkinje cells but also ectopically expressed specifically in lymphoma cells of patients with RGS8-related ACA. The present results and those of the four cases previously described suggest that RGS8-Abs define a new paraneoplastic neurological syndrome of extreme rarity found mostly in middle-aged males that associates pure cerebellar ataxia and a particular lymphoma specifically expressing the RGS8 antigen. As in other paraneoplastic ACA with intracellular antigen, the disease course is severe, and patients tend to exhibit a poor response to immune therapy.

01 Sep 2024·Redox Biology

Redox-modulated SNX25 as a novel regulator of GPCR-G protein signaling from endosomes

Article

Author: Sun, Mingwei ; Zhang, Xiaofei ; Du, Ruyue ; Zhang, Yulong ; Xu, Tingting ; Dai, Qiankun ; Xu, Jinxin ; Liu, Jinsong ; Yin, Menghui ; Dong, Yan ; Yu, Zhijun ; Liu, Cuicui ; Gao, Hanhan

GPCR-G protein signaling from endosomes plays a crucial role in various physiological and pathological processes. However, the mechanism by which endosomal G protein signaling is terminated remains largely unknown. In this study, we aimed to investigate the regulatory mechanisms involved in terminating the signaling of Gα subunits from endosomes. Through structural analysis and cell-based assays, we have discovered that SNX25, a protein that targets endosomes via its PXA or PXC domain, interacts with regulator of G protein signaling (RGS) proteins (including RGS2, RGS4, RGS8, and RGS17) in a redox-regulated manner. The interaction between SNX25 and these RGS proteins enhances their GTPase-accelerating activity towards Gα_i/q and their ability to bind GDP-bound (inactive form) Gα_i/q. As a result, SNX25 recruits these RGS proteins to endosomes, leading to the termination of endosomal Gα_i/q signaling. Furthermore, we have found that the SNX25/RGS complex also exerts a negative regulatory effect on Gα_i/q signaling from the plasma membrane. This is achieved by recruiting Gα_i/q to endosomes and preventing its activation on the plasma membrane. Our findings shed light on the previously unknown role of redox-modulated SNX25 in inhibiting Gα_i/q signaling, thereby uncovering a novel mechanism for terminating Gα_i/q signaling from endosomes. Importantly, this study expands our understanding of the regulation of GPCR-Gα_i/q signaling beyond the plasma membrane.

01 May 2024·Thoracic Cancer

Identification of a risk score model based on tertiary lymphoid structure‐related genes for predicting immunotherapy efficacy in non‐small cell lung cancer

Article

Author: Liu, Jia-Qi ; Zhou, Qing ; Deng, Yu ; Xu, Chong-Rui ; Peng, Ying-Long ; Luo, Wei-Chi ; Huang, Zi-Jian ; Mei, Shi-Qi ; Chen, Zhi-Hong

AbstractBackgroundTertiary lymphoid structures (TLSs) affect the prognosis and efficacy of immunotherapy in patients with non‐small cell lung cancer (NSCLC), but the underlying mechanisms are not well understood.MethodsTLSs were identified and categorized online from the Cancer Digital Slide Archive (CDSA). Overall survival (OS) and disease‐free survival (DFS) were analyzed. GSE111414 and GSE136961 datasets were downloaded from the GEO database. GSVA, GO and KEGG were used to explore the signaling pathways. Immune cell infiltration was analyzed by xCell, ssGSEA and MCP‐counter. The analysis of WGCNA, Lasso and multivariate cox regression were conducted to develop a gene risk score model based on the SU2C‐MARK cohort.ResultsTLS‐positive was a protective factor for OS according to multivariate cox regression analysis (p = 0.029). Both the TLS‐positive and TLS‐mature groups exhibited genes enrichment in immune activation pathways. The TLS‐mature group showed more activated dendritic cell infiltration than the TLS‐immature group. We screened TLS‐related genes using WGCNA. Lasso and multivariate cox regression analysis were used to construct a five‐genes (RGS8, RUF4, HLA‐DQB2, THEMIS, and TRBV12‐5) risk score model, the progression free survival (PFS) and OS of patients in the low‐risk group were markedly superior to those in the high‐risk group (p < 0.0001; p = 0.0015, respectively). Calibration and ROC curves indicated that the combined model with gene risk score and clinical features could predict the PFS of patients who have received immunotherapy more accurately than a single clinical factor.ConclusionsOur data suggested a pivotal role of TLSs formation in survival outcome and immunotherapy response of NSCLC patients. Tumors with mature TLS formation showed more activated immune microenvironment. In addition, the model constructed by TLS‐related genes could predict the response to immunotherapy and is meaningful for clinical decision‐making.

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RGS8

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