RGS4

Last update 08 May 2025

Basic Info

Synonyms

regulator of G protein signaling 4, regulator of G-protein signaling 4, regulator of G-protein signalling 4

+ [4]

Introduction

Inhibits signal transduction by increasing the GTPase activity of G protein alpha subunits thereby driving them into their inactive GDP-bound form. Activity on G(z)-alpha is inhibited by phosphorylation of the G-protein. Activity on G(z)-alpha and G(i)-alpha-1 is inhibited by palmitoylation of the G-protein.

100 Clinical Results associated with RGS4

100 Translational Medicine associated with RGS4

0 Patents (Medical) associated with RGS4

707

Literatures (Medical) associated with RGS4

01 Jun 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Silencing RGS7 attenuates atrial fibrillation progression by activating the cGMP-PKG signaling pathway

Article

Author: Huang, Hao ; Zeng, Jie ; Xiong, Yan

BACKGROUNDAtrial fibrillation (AF) is a common diagnosed heart disease that needs novel managements. This study aimed to seek potential biomarkers and underlying regulatory pathways associated with AF.METHODSDifferential expressed genes (DEGs) were identified from the Gene Expression Omnibus database, followed by a protein-protein interaction (PPI) network to discover hub genes. Principal components analysis (PCA) and receiver operating characteristic (ROC) curves were performed to evaluate the ability of hub genes to discriminate between AF and control. RGS7 was selected as a key hub gene, and genes co-expressed with RGS7 were identified for functional enrichment analysis. Further in vivo and in vitro experiments were conducted to investigate the effects of silencing RGS7 on AF and the potential pathway.RESULTSWe identified top 5 hub genes (RGS7, EGFR, RGS4, GNA13 and RGS11) from the PPI network. PCA showed these genes could distinguish between AF and control samples, with 100 % of the area under curve (AUC) values. Silencing RGS7 inhibited cell apoptosis, inflammation and oxidative stress, and increased mitochondrial membrane potential in angiotensin II (AngII)-treated HL-1 cells, while overexpression of RGS7 reversed the inhibitory effects of silencing RGS7 on AF. Additionally, silencing RGS7 improved cardiac function and decreased cardiac fibrosis in AF rats. The cGMP-PKG signaling pathway was screened as a potential signal transduction pathway, and silencing RGS7 increased the expression of PKG1, while KT5823 blocked the process.CONCLUSIONSilencing RGS7 attenuates AF by activating the cGMP-PKG signaling pathway, which may offer directions for selecting biomarkers and regulatory pathways for AF.

01 May 2025·Neurobiology of Disease

Joint analysis of single-cell RNA sequencing and bulk transcriptome reveals the heterogeneity of the urea cycle of astrocytes in glioblastoma

Article

Author: Chen, Huahui ; Wan, Xing ; Tong, Minfeng ; Tu, Qi ; Xu, Zhijian ; Wang, Lude

BACKGROUNDGlioblastoma (GB) is incurable with a dismal prognosis. Single-cell RNA sequencing (scRNA-seq) is a pivotal tool for studying tumor heterogeneity. The dysregulation of the urea cycle (UC) frequently occurs in tumors, but its characteristics in GB have not been illuminated. This study integrated scRNA-seq UC scores and bulk RNA-seq data to build a GB prognostic model.METHODSSamples from 3 pairs of GB patients were collected for scRNA-seq analysis. GB-mRNA expression data, clinical data, and SNV mutation data were sourced from the Cancer Genome Atlas (TCGA). GB-mRNA expression data and clinical data were downloaded from the Chinese Glioma Genome Atlas (CGGA). GB RNA-seq data and clinical data were obtained from Gene Expression Omnibus (GEO) database. The R package Seurat was applied for scRNA-seq data processing. UMAP and TSNE were used for dimensionality reduction. UCell enrichment method was employed to score each astrocyte. Monocle algorithm was applied for pseudotime trajectory analysis. CellChat R package was applied for cell communication analysis. Cell labeling was performed on the results of the nine subclusters of astrocytes. The GSE138794 dataset was used to validate the results of single-cell classification. For bulk RNA-seq, univariate Cox and LASSO analyses were undertaken to screen prognostic genes, while multivariate Cox regression analysis was applied to set up a prognostic model. The differences between high-risk (HR) and low-risk (LR) groups were studied in terms of immune infiltration, sensitivity to anti-tumor drugs, etc. We verified the effect of the marker gene on the function of GB cells at the cellular level.RESULTSThe analysis of scRNA-seq data yielded 7 core cell types. Further clustering of the largest proportion of astrocytes resulted in 9 subclusters. UC score and pseudotime analysis revealed the heterogeneity and differentiation process among subclusters. Subcluster 8 was annotated as an immature astrocyte (marker: CXCL8), and this cell cluster had a higher UC score. The results were validated in the GSE138794 dataset. Combining UC scores, we performed univariate Cox and LASSO to select prognostic genes on bulk RNA-seq data. A prognostic model based on 5 feature genes (RGS4, CTSB, SERPINE2, ID1, and CALD1) was established through multivariate Cox analysis. In addition, patients in the HR group had higher immune infiltration and immune function. Final cell experiments demonstrated that 5 feature genes were highly expressed in GB cells. CALD1 promoted the malignant phenotype of GB cells.CONCLUSIONWe set up a novel prognostic model for predicting the survival of GB patients by integrating bulk RNA-seq and scRNA-seq data. The risk score was closely correlated with immune infiltration and drug sensitivity, pinpointing it as a promising independent prognostic factor.

01 Mar 2025·Chemical Biology & Drug Design

Ailanthone Restrains Osteosarcoma Growth and Metastasis by Decreasing the Expression of Regulator of G Protein Signaling 4 and Twist Family BHLH Transcription Factor 1

Article

Author: Shi, Qiaojing ; Liu, Hongzhan ; Tan, Qiang

ABSTRACTTraditional Chinese medicine Ailanthone (AIL) has been confirmed to possess antimalarial, anti‐inflammatory, and anticancer effects. Here, this study aimed to excavate the biological role and mechanism of AIL on osteosarcoma (OS) progression. Levels of Regulator of G protein signaling 4 (RGS4) and Twist Family BHLH Transcription Factor 1 (TWIST1) were detected by qRT‐PCR and western blotting. In vitro and tumor formation experiments were conducted for functional analysis. The protein interaction between RGS4 and TWIST1 was verified by using a Co‐immunoprecipitation assay. AIL impeded the proliferation, invasion, migration, and epithelial‐mesenchymal transition (EMT) progression, but induced apoptosis in OS cells. RGS4 was highly expressed in OS tissues and cells and was decreased by AIL in cells. RGS4 silencing suppressed the growth and metastasis of OS cells, and RGS4 overexpression reversed the anticancer action of AIL in OS cells. Mechanistically, RGS4 interacted with TWIST1 and positively regulated its expression. TWIST1 was highly expressed in OS tissues and cells and could be reduced by AIL in cells. Moreover, TWIST1 overexpression abolished RGS4 silencing‐triggered growth and metastasis inhibition in OS cells. Importantly, AIL impeded OS growth and metastasis in vivo by regulating RGS4 and TWIST1. Ailanthone restrained OS growth and metastasis by decreasing RGS4 and TWIST1 expression.

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RGS4

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