RGS17 Antibody - C-terminal region (ARP34049_P050)
- Known as:
- RGS17 Antibody - C-terminal region (ARP34049_P050)
- Catalog number:
- arp34049_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RGS17 Antibody - C-terminal region (ARP34049_P050)
Related genes to: RGS17 Antibody - C-terminal region (ARP34049_P050)
- Gene:
- RGS17 NIH gene
- Name:
- regulator of G protein signaling 17
- Previous symbol:
- -
- Synonyms:
- RGSZ2, RGS-17
- Chromosome:
- 6q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-29
- Date modifiied:
- 2017-04-13
Related products to: RGS17 Antibody - C-terminal region (ARP34049_P050)
Related articles to: RGS17 Antibody - C-terminal region (ARP34049_P050)
- The Regulator of G Protein Signaling (RGS) gene family, known as critical negative regulators of G protein-coupled receptor (GPCR) signaling pathways, has emerged as a potential therapeutic target in various malignancies. This study aims to comprehensively evaluate the expression profiles of RGS genes in breast cancer, exploring their diagnostic, prognostic, and chemotherapeutic sensitivity-related roles. - Source: PubMed
Publication date: 2025/11/22
Wang HuanhuanFeng MingHuang HongZhang XiaoqingYao Chang - The article "MiRNA-199 inhibits malignant progression of lung cancer through mediating RGS17" by W.-Z. Su, L.-F. Ren published in Eur Rev Med Pharmacol Sci 2019; 23 (8): 3390-3400-DOI: 10.26355/eurrev_201904_17703-PMID: 31081094 has been retracted in accordance with the Publisher and the Editor in Chief. Following some concerns raised on PubPeer (https://pubpeer.com/publications/2E8256B0FA92987A3510C854E633DA), the Journal has started an investigation to assess the validity of the results as well as possible figure manipulation. The journal's investigation identified multiple instances of figure duplication, specifically in panel E of Figure 2 and in the Western blots of Figure 4, which appear to overlap with images from previously published articles. In addition, a duplication was detected within panel C of Figure 5. The authors were contacted and informed of the ongoing investigation, and were requested to provide the original data supporting the manuscript. The authors responded that, due to their relocation and lack of access to the original computer files, the underlying data could not be retrieved. As a result, the Journal has decided to retract this article. This article has been retracted. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17703. - Source: PubMed
Su W-ZRen L-F - The tumor immune microenvironment (TIME) and its impact on the prognoses and treatment of lung adenocarcinoma (LUAD) represent a major focus of research in this field. The present study primarily elucidates the role of RGS17 in TIME of LUAD. - Source: PubMed
Publication date: 2025/07/08
Lou MingTong Ji-ChunWu Qi-YongZhu ZhengMao Xiao-LiangLu Jia-Wei - Fibromyalgia (FM) is a complex autoimmune disorder characterized by widespread pain and fatigue, with significant diagnostic challenges due to the absence of specific biomarkers. This study aims to identify and validate potential genetic markers for FM to facilitate earlier diagnosis and intervention. - Source: PubMed
Publication date: 2025/04/17
Zhao FuyuZhao JiananLi YangSong ChenyangCheng YaxinLi YunshenWu ShiyaHe BinghengJiao JuanChang Cen - Cisplatin is a chemotherapy drug used to treat different solid tumors, including ovarian, bladder, lung, and head and neck cancers. One of its significant side effects is ototoxicity, especially when high doses are required. Cisplatin-induced ototoxicity is associated with increased cochlear cell death resulting from DNA damage, caspase activation, oxidative stress, inflammation, and glutamate excitotoxicity. The regulator of G protein signaling 17 (RGS17), a member of the RGS-RZ subfamily, hastens the hydrolysis of GTP to GDP on the G subunit. In the current study, we demonstrate the role of in cisplatin-induced cochlear inflammation and ototoxicity. C57BL/6J mice treated with two cycles of cisplatin (3.5 mg/kg) showed a significant elevation in ABR thresholds, along with loss of outer hair cells and inner hair cells synapse. Furthermore, immunohistochemical analysis revealed that cisplatin administration upregulates CXCL1, accompanied by an increase in the number of CD45 and CD68-positive immune cells. On the other hand, knockout in hair cells protects against cisplatin-induced elevation of ABR thresholds, outer hair cell loss, cochlear inflammation, and inner hair cell synaptopathy. Moreover, knockout downregulates CXCL1 immunolabeling and decreases the number of CD45 and CD68-positive immune cells induced by cisplatin. These results suggest that is implicated in cisplatin ototoxicity, potentially by initiating the immune cascade, and indicate as a relevant target for treating cisplatin ototoxicity. - Source: PubMed
Publication date: 2025/02/21
Al Aameri Raheem F HAlanisi Entkhab M AAl Sallami DheyaaAlberts IanTischkau ShelleyRybak Leonard PRamkumar Vickram