GPR_40 (280_300)(Human) _ 100ug
- Known as:
- GPR_40 (280_300)(Human) _ 100ug
- Catalog number:
- 001-68
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Phoenix Peptide
- Gene target:
- GPR_40 (280_300)(Human) _ 100ug
Related genes to: GPR_40 (280_300)(Human) _ 100ug
- Gene:
- FFAR1 NIH gene
- Name:
- free fatty acid receptor 1
- Previous symbol:
- GPR40
- Synonyms:
- FFA1R
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-10
- Date modifiied:
- 2016-10-05
Related products to: GPR_40 (280_300)(Human) _ 100ug
Related articles to: GPR_40 (280_300)(Human) _ 100ug
- Melanoma, a highly malignant skin cancer, has seen a rising incidence and death toll. MRGPRF is a novel melanoma suppressor that inhibits the PI3K/AKT pathway. However, the regulation of MRGPRF in melanoma remains unclear. Here, 40 ubiquitin-specific proteases (USPs) are screened and USP45 is identified as a significant stabilizer of MRGPRF. Immunohistochemistry on melanoma patient biopsies demonstrates that USP45 expression is markedly reduced in melanoma tissues compared to adjacent noncancerous epidermis. Bioinformatic analyses corroborate that USP45 mRNA levels are downregulated in melanoma, and low USP45 expression is associated with poor patient prognosis. Functional assays demonstrate that USP45 overexpression inhibits melanoma cell malignancy, whereas USP45 knockdown promotes it. Mechanistically, USP45's catalytic domain directly binds to the N-terminal of MRGPRF and stabilizes MRGPRF, likely by removing its K63-linked ubiquitination in melanoma cells. The antimelanoma effects of USP45 are mitigated by MRGPRF depletion, while MRGPRF overexpression rescues the enhanced malignant phenotype induced by USP45 deficiency. In vivo, a melanoma xenograft mouse model shows that USP45 overexpression significantly impairs melanoma progression. These findings establish USP45 as a melanoma suppressor, at least partially through its stabilization of MRGPRF, highlighting a novel mechanism in melanoma pathogenesis and suggesting that USP45 agonists may serve as potential therapeutic agents. - Source: PubMed
Publication date: 2025/08/11
Zhang WancongChen LiyunZhao JingMa AiweiShi WenqiZhang YiwenTang ZixuanGuo JiaruiXu ZaihuaZhou JiandaTang Shijie - The gut microbiota has been linked to a number of neurological disorders. However, it is unclear whether the gut microbiota is involved in the genesis of chronic itch, a refractory condition that afflicts patients both physically and mentally. Here, we report that depletion of gut microbiota enhances tolerance to itch in mice orally administered with antibiotics (ABX) and mice free of germ. Of note, oral gavage with (), a prominent species of the genus with most differential change, corrected the ABX-induced itch dysfunction through its driven metabolite acetyl-l-carnitine (ALC). Mechanistically, gut microbiota or depletion caused a decrease in RNA N6-methyladenosine (mA) demethylase FTO expression in the dorsal horn and a consequent increase in RNA mA sites in Mas-related G protein-coupled receptor F () mRNA, leading to decreased MRGPRF protein. The downregulation of FTO was triggered by inactivation of ETS proto-oncogene 1 (ETS1), a transcription factor that binds to the promoter. These findings support a gut microbe - spinal connection in modulation of itch sensation in RNA mA epigenetic-dependent manner and highlight a critical role of ALC in linking the altered and itch dysfunction. - Source: PubMed
Publication date: 2025/04/27
Jin TongLi Si-YuanZheng Hong-LiLiu Xiao-DanHuang YueMa GanZhao Ya-XuanZhao Xiao-TianYang LiWang Qi-HuiWang Hong-JunGu ChengyongPan ZhiqiangLin Fuqing - Malignant melanoma (MM) is a malignant tumor associated with high mortality rates and propensity for metastasis. Despite advancement in treatment, the incidence of MM continue to rise globally. GPR168, also known as MrgprF, is a MAS related GPR family member. The low expression of GPR168 has also been reported in many malignant tumors including MM. In the study, the statistical analysis from The Cancer Genome Atlas (TCGA) revealed a significant down regulation of GPR168 in melanoma compared to normal melanocytes, underscoring its importance in MM. The aim of the present study is to investigate the affect of GPR168 overexpression and elucidate its molecular mechanisms in MM cells. In addition, we used mouse melanoma B16-F10 cell line and xenograph tumor model to explore the function of GPR168 in melanoma. Our findings demonstrate that GPR168 overexpression could inhibit B16-F10 cell proliferation, migration, and xenografts tumor growth. Further, mechanistic studies revealed that GPR168 affected B16-F10 progress through Akt signal pathway with the decreased expression of p-Akt, p-GSK-3β, β-catenin, Myc, CyclinD1 and CDK4. In order to validate these findings, a rescue experiment was formulated employing GPR168 polyclonal antibody (Anti-GPR168 pAbs) to block GPR168 functionality. The addition of Anti-GPR168 pAbs into the culture medium restored both cell proliferation and migration. In conclusion, the overexpression of GPR168 in mouse melanoma B16-F10 cells suppressed proliferation and migration through the Akt signaling pathway. These findings collectively propose GPR168 as a promising novel tumor suppressor in MM, suggesting its potential as a therapeutic target in future interventions. - Source: PubMed
Publication date: 2024/05/28
Guo XiangGuo ZongliangBai PeirongGuo CongfangLiu XueweiZhu KaiyiLi XiaoyanZhao Yiyan - G protein-coupled receptors (GPCRs) modulate the function of adipose tissue (AT) in general and of adipocytes, specifically. Although it is well-established that GPCRs are widely expressed in AT, their repertoire as well as their regulation and function in (patho)physiological conditions (e.g., obesity) is not fully resolved. Here, we established FATTLAS, an interactive public database, for improved access and analysis of RNA-seq data of mouse and human AT. After extracting the GPCRome of non-obese and obese individuals, highly expressed and differentially regulated GPCRs were identified. Exemplarily, we describe four receptors (GPR146, MRGPRF, FZD5, PTGER2) and analyzed their functions in a (pre)adipocyte cell model. Besides all receptors being involved in adipogenesis, MRGPRF is essential for adipocyte viability and regulates cAMP levels, while GPR146 modulates adipocyte lipolysis via constitutive activation of Gi proteins. Taken together, by implementing and using FATTLAS we describe four hitherto unrecognized GPCRs associated with AT function and adipogenesis. - Source: PubMed
Publication date: 2023/09/09
Kaczmarek IsabellWower IsabelEttig KatjaKuhn Christina KatharinaKraft RobertLandgraf KathrinKörner AntjeSchöneberg TorstenHorn SusanneThor Doreen - Ferroptosis, a newly discovered mode of cell death, emerges as a new target for atherosclerosis (AS). Long noncoding RNAs (lncRNAs) are involved in the regulation of ferroptosis. In our previous study, lnc-MRGPRF-6:1 was highly expressed in patients with coronary atherosclerotic disease (CAD) and closely associated with macrophage-mediated inflammation in AS. In the present study, we aim to investigate the role of lnc-MRGPRF-6:1 in oxidized-low-density lipoprotein (ox-LDL)-induced macrophage ferroptosis in AS. - Source: PubMed
Publication date: 2023/08/16
You ZhihuanYe XiaotianJiang MeihuaGu NingLiang Caihong