RGS4 antibody - C-terminal region (ARP30213_P050)
- Known as:
- RGS4 (anti-) - C-terminal region (ARP30213_P050)
- Catalog number:
- arp30213_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RGS4 antibody - C-terminal region (ARP30213_P050)
Related genes to: RGS4 antibody - C-terminal region (ARP30213_P050)
- Gene:
- RGS4 NIH gene
- Name:
- regulator of G protein signaling 4
- Previous symbol:
- SCZD9
- Synonyms:
- -
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-09
- Date modifiied:
- 2017-04-13
Related products to: RGS4 antibody - C-terminal region (ARP30213_P050)
Related articles to: RGS4 antibody - C-terminal region (ARP30213_P050)
- Angiogenesis is critical for post-ischemic tissue repair. Although miR-485-5p is highly expressed in vascular tissues and RGS4 regulates angiogenesis, their specific roles under hypoxia remain largely unknown. This study aimed to elucidate these functions and underlying mechanisms. Using a CoCl₂-induced hypoxic model in HUVECs, we observed that hypoxia significantly downregulated miR-485-5p expression while concurrently upregulating RGS4 mRNA levels. Notably, either inhibition of RGS4 or overexpression of miR-485-5p markedly enhanced HUVEC proliferation, migration, and tube formation. A luciferase reporter assay further confirmed that miR-485-5p directly targets RGS4. In addition, miR-485-5p overexpression or RGS4 inhibition increased the phosphorylation levels of VEGFR-2, AKT, and ERK1/2. Through co-immunoprecipitation assays, we revealed for the first time a direct interaction between RGS4 and VEGFR-2, which suppresses VEGF signaling and consequently impairs angiogenesis. Conversely, overexpression of RGS4 reversed the pro-angiogenic effects of miR-485-5p, as evidenced by reduced VEGFR-2/AKT/ERK1/2 phosphorylation and decreased proliferation, migration, and tube formation in HUVECs. These findings indicate that miR-485-5p promotes angiogenesis by downregulating RGS4. Consistent with these in vitro results, experiments in vivo using a rat hindlimb ischemia model confirmed that inhibition of RGS4 via si-RGS4 or overexpression of miR-485-5p via agomir-miR-485-5p markedly improved blood perfusion recovery, enhanced vascular angiogenesis, and increased VEGFR-2/AKT/ERK1/2 phosphorylation. Collectively, our study demonstrates that the miR-485-5p/RGS4 axis promotes hypoxia-induced angiogenesis by relieving RGS4-mediated inhibition of VEGFR-2/AKT/ERK1/2 signaling, thereby providing a strong rationale for targeting miR-485-5p as a possible treatment approach for lower extremity arterial disease. - Source: PubMed
Publication date: 2026/08/12
Li MengtingLuo YulinLi YufeiYou JingcanWang LiqunWu JianboZheng YoukunLuo Mao - The SNPs in the 5' regulatory region of the human RGS4 gene were reportedly associated with schizophrenia risk. - Source: PubMed
Publication date: 2026/08/01
Xu Feng-LingYang Xin-RuiYang Yan-YanWang Rong-ShuaiLiu Li - Breast cancer (BC) is a heterogeneous malignancy with diverse molecular subtypes and variable clinical outcomes. Despite diagnostic and therapeutic advances, recurrence and metastasis contribute to poor prognosis in subsets of patients. Regulators of G protein signaling (RGS) proteins, negative modulators of G protein-coupled receptor (GPCR) pathways, influence tumor progression, but their expression profiles, genomic alterations, immune associations, and prognostic roles in BC remain incompletely understood. This study systematically investigated the RGS family to identify potential biomarkers and therapeutic targets. - Source: PubMed
Mirzaei ZohrehMoghaddam Madiheh MazaheriBarati TaherehEbrahimi AmirKhaniani Mahmoud Shekari - Alzheimer's disease (AD) is characterized by progressive neurodegeneration in regionally vulnerable brain areas, yet molecular insights into early pathogenic mechanisms remain limited. - Source: PubMed
Publication date: 2026/06/01
Jaberi Khojaste RahimiAlashti Shayan KhaliliHooshmandi SedigheVatankhah PooyaHaghighi Maryam RohaniSavardashtaki AmirAligholi HadiJaberi Abbas Rahimi - The mechanisms underlying kidney repair remain incompletely understood. GATA6-expressing large cavity macrophages are reported to facilitate inflammation resolution and repair in several organs following injury, but their role in kidney disease is unknown. GATA6 expression was minimal in normal mouse and human kidney. Across three experimental kidney disease models (ischemia-reperfusion injury, unilateral ureteric obstruction and nephrotoxic serum glomerulonephritis), GATA6 expression increased progressively in the renal interstitium with chronic, but not acute injury. Immunophenotyping demonstrated that GATA6 + cells mainly expressed stromal markers (RGS4, PDGFRβ, αSMA) as opposed to leukocyte markers (CD45, F4/80, MHC-II). Single-cell RNA sequencing confirmed enrichment of Gata6 expression in kidney stromal cell populations. GATA6 + cells expressed genes associated with stromal cell identity, repair, inflammation, angiogenesis and collagen biosynthesis. In human kidney biopsies from patients with hypertensive nephrosclerosis and IgA nephropathy, interstitial GATA6 expression was increased and correlated with the degree of fibrosis. As in mice, human GATA6 + cells were largely CD45 and MHC-II negative but expressed stromal markers, consistent with non-immune interstitial cells rather than macrophages. Together, these findings demonstrate that GATA6 is predominantly expressed by kidney stromal cells with limited evidence of a major role for GATA6 + large cavity macrophages in kidney injury and repair. - Source: PubMed
Publication date: 2026/07/09
Belay Sisay GetieElias Esteban ELau ArthurAndonegui GracielaChapman KevinChun JustinMuruve Daniel A