RGS16

Last update 08 May 2025

Basic Info

Synonyms

A28-RGS14, A28-RGS14P, hRGS-r

+ [8]

Introduction

Regulates G protein-coupled receptor signaling cascades. Inhibits signal transduction by increasing the GTPase activity of G protein alpha subunits, thereby driving them into their inactive GDP-bound form (PubMed:11602604, PubMed:18434541). Plays an important role in the phototransduction cascade by regulating the lifetime and effective concentration of activated transducin alpha. May regulate extra and intracellular mitogenic signals (By similarity).

100 Clinical Results associated with RGS16

100 Translational Medicine associated with RGS16

0 Patents (Medical) associated with RGS16

215

Literatures (Medical) associated with RGS16

16 Feb 2024·Medicine

Status and trends of RGS16 based on data visualization analysis: A review

Review

Author: Gongchang, Yu ; Yuanzhen, Chen ; Bin, Shi ; Liangyu, Xie ; Zhiyong, Lu ; Wenbo, Liu

G-protein signaling regulator 16 (RGS16) has been confirmed that RGS16 is associated with cancer, neurodegenerative diseases, and cardiovascular diseases. Moreover, many studies have shown that RGS16 can be used as a biomarker for cancer diagnosis and prognosis. We used CiteSpace and VOS viewer software to perform a bibliometric analysis of 290 publications in the core collection of Web of Science. All the articles come from 399 institutions, including 618 authors, 179 journals, 40 countries, 115 keywords, 1 language, two types of papers, and reviews. The United States has the largest number of publications. The Research Center of Allergy and Infectious Diseases (NIAID) publishes the most papers, Emory University is the most recent of all institutions with the most recent results in the RGS16 study. Cell biology is the most studied discipline, and the most studied topic is migration. Drury published RGS16-related articles with the most citations (n = 15), and Berman published articles with the most citations (n = 106). The biological applications of RGS16 are currently a hot area of RGS16 research, including inflammation, cancer, ulcerative colitis, metabolic acidosis, platelet activation, and thrombosis. The current scientometrics study provides an overview of RGS16 research from 1995 to 2022. This study provides an overview of current and potential future research hotspots in the field of RGS16 and can be used as a resource for interested researchers.

01 Feb 2024·Journal of Molecular Medicine

Phosphorylation of RGS16 at Tyr168 promote HBeAg-mediated macrophage activation by ERK pathway to accelerate liver injury

Article

Author: Wu, Nijin ; Bian, Hongjun ; Tian, Miaomiao ; Cao, Huiling ; Liu, Tiantian ; Ma, Shujun ; Xie, Xiaoyu ; Liu, Chenxi ; Qi, Jianni ; Wang, Le ; You, Yajing

Liver injury is closely associated with macrophage activation following HBV infection. Our previous study showed that only HBeAg, but not HBsAg and HBcAg, stably enhances inflammatory cytokine production in macrophages. And we also indicated that HBeAg could induce macrophage activation via TLR2 and thus aggravate the progression of liver fibrosis. However, the specific molecular mechanism of HBeAg in macrophage activation is not clear. We screened significantly overexpressed RGS16 from RNASeq results of HBeAg-stimulated macrophages and validated them with cellular assays, GSE83148 microarray dataset, and in clinical samples. Meanwhile, small interference, plasmid, and lentivirus transfection assays were used to establish cell models for knockdown and overexpression of RGS16, and q-PCR, ELISA, Transwell, and CCK-8 assays were used to analyze the role of RGS16 in HBeAg-induced macrophage activation. In addition, the upstream and downstream mechanisms of RGS16 in HBeAg-treated macrophage activation were explored using inhibitors, phostag gels, and RGS16 phosphorylation mutant plasmids. Finally, the effect of RGS16 on hepatic inflammation in murine tissues was evaluated by H&E staining, liver enzyme assay and immunofluorescence. RGS16 was significantly upregulated in HBeAg-induced macrophage activation, and its expression was enhanced with increasing HBeAg content and treatment time. Functional experiments showed that overexpression of RGS16 promoted the production of inflammatory factors TNF-α and IL-6 and boosted macrophage proliferation and migration, while knockdown of RGS16 exhibited the opposite effect. Mechanistically, we discovered that RGS16 is regulated by the TLR2/P38/STAT5 signaling pathway. Meanwhile, RGS16 enhanced ERK phosphorylation via its own Tyr168 phosphorylation to contribute to macrophage activation, thereby accelerating liver injury. Finally, in mice, overexpression of RGS16 markedly strengthened liver inflammation. HBeAg upregulates RGS16 expression through the TLR2-P38-STAT5 axis, and the upregulated expression of RGS16 enhances macrophage activation and accelerates liver injury by promoting ERK phosphorylation. In this process, phosphorylation of Tyr168 is necessary for RGS16 to function. KEY MESSAGES: RGS16 boosted HBeAg-induced macrophage inflammation, proliferation, and migration. Tyr168 phosphorylation of RGS16 affected by ERK promoted macrophage activation. HBeAg upregulated the expression of RGS16 through TLR2/P38/STAT5 signal pathway. RGS16 promoted liver injury by regulating macrophage functions in mouse model.

01 Oct 2023·International journal of radiation oncology, biology, physics

HPK1 Inhibition Enhancing HFRT Anti-Tumor Immune Response.

Article

Author: Zhang, J ; Wang, F ; Shang, S ; Ren, Z ; Ma, J ; Chen, D ; Wu, M ; Ma, Y ; Zhang, Y ; Yu, J ; Yan, W

PURPOSE/OBJECTIVE(S)Radiation therapy, as one of the canonical treatments for classic tumors, results in impressive clinical responses. Stereotactic body radiotherapy (SBRT) has been increasingly used as one main therapy in early-stage non-small-cell lung cancer (NSCLC). SBRT affords good local tumor control, however, recurrence and metastasis are still the main causes of treatment failure. With the continuous deepening of the relationship between radiotherapy (RT) and immunity, reversing RT induced immunosuppression is considered to be a promising strategy to improve radiotherapy efficacy. Hematopoietic progenitor kinase 1 (HPK1) is mainly expressed in immune cells while rarely expressed in tumor cells. It has been proven to play a negative regulatory role in T cell receptor (TCR) signal. Therefore, we hypothesized that the combination of HPK1 inhibitor with SBRT would boost local and systemic anti-tumor immune responses by potentiating the anti-tumor effects of SBRT.MATERIALS/METHODSUsing Digital Spatial Profiler (DSP), we analyzed HPK1 expression in the tumor specimens of 39 NSCLC patients treated with SBRT. By establishing mice subcutaneous tumor models, we assessed the combination of a HPK1 inhibitor and local hyper-fractionated radiotherapy (HFRT) on local and systemic tumor control and mouse survival. Using Single-cell RNA sequencing, Flow cytometry and pharmacological treatment, we analyzed and verified Tumor-infiltrating lymphocytes (TILs), and excavated the specific mechanism of the HPK1 inhibitor enhancing HFRT -induced anti -tumor immune response.RESULTSIn the tumor specimens of NSCLC patients treated with SBRT, we found that high expression HPK1 in TILs predicted poor progression-free survival (PFS). Among the C57BL/6 mice model, HFRT combined with a HPK1 inhibitor promoted local response, and improved the survival rate of mice, showing better anti-tumor curative effects. We further showed that HFRT promoted CD8+ T cell cytotoxic activity, and also aggravated CD8+ T cell exhaustion. After the intervention of HPK1 small molecular inhibitors, the proportion of exhaustion CD8+T cells was significantly reduced, while CD8+T cell cytotoxic activity was further enhanced in the later period. Single-cell RNA sequencing and pharmacological inhibition of HPK1 revealed that HPK1 mediated the exhaustion of CD8+T cells by regulating RGS16. In abscopal effects preclinical models, BGB-15025 induced obvious abscopal effect.CONCLUSIONThus, we demonstrate that HPK1 mediates HFRT-induced CD8+T cell exhaustion by regulating RGS16, and HPK1 is an attractive drug target for enhancing local and systemic radiotherapy.

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RGS16

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