MRP5
- Known as:
- MRP5
- Catalog number:
- Y214183
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MRP5
Related genes to: MRP5
- Gene:
- ABCC5 NIH gene
- Name:
- ATP binding cassette subfamily C member 5
- Previous symbol:
- -
- Synonyms:
- MRP5, SMRP, EST277145, MOAT-C
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2016-10-05
Related products to: MRP5
Related articles to: MRP5
- Dysregulation of efflux ATP-binding cassette (ABC) transporters often confers multidrug resistance, presenting significant challenges in treating various diseases (eg, hepatocellular carcinoma [HCC]). The let-7-5p microRNAs (miRNAs), commonly downregulated in HCC, have established roles in controlling post-transcriptional gene regulation of ABC transporters (eg, multidrug resistance-associated protein 5 MRP5/ABCC5) and some oncogenes (eg, RNA-binding protein LIN28B). Although previous research has demonstrated the potential of particular let-7-5p isoforms to regulate ABC transporters and inhibit HCC cell viability, the comparative efficacy of let-7-5p isoforms whose sequences differ in several nucleosides is unknown. This study was to compare the effectiveness of 7 major let-7-5p isoforms (let-7a to let-7g) to regulate ABCC5 and LIN28B targets and inhibit HCC cell viability in vitro by using novel bioengineered RNA let-7-5p (BioRNA/let-7-5p) agents. Release of let-7-5p isoforms from individual BioRNA/let-7-5p molecules in Huh7, HepG2, and Hep3B cells was validated. Efficacy of BioRNA/let-7-5p isoforms to repress ABCC5/MRP5 and LIN28B protein levels was found to be target dependent; among them, let-7c and let-7d-5p exhibited broader regulatory efficacy against ABCC5/MRP5, while let-7d-5p emerged as the most potent suppressor of LIN28B, generally in accordance with let-7-5p abundance and target complementarity. By contrast, let-7-5p isoforms showed minimal impact on ABCC2/MRP2 and ABCC4/MRP4 protein levels. In addition, let-7-5p isoforms showed variable efficacy to inhibit the viability of different HCC cells. Together, our studies established the functional differences of let-7-5p isoforms in regulating target gene expression and inhibiting HCC cell viability, providing insights into intrinsic differences of miRNA isoforms to inform rational development of miRNA therapeutics or combination therapy. SIGNIFICANCE STATEMENT: Using novel bioengineered RNA agents, this study established the functional differences of 7 major human let-7-5p isoforms to control target gene expression and hepatocellular carcinoma cell viability in vitro. These findings demonstrate the potential of bioengineered RNA molecules to interrogate post-transcriptional gene regulation mechanisms, highlighting specific let-7-5p isoforms to modulate transporter and oncogene expression toward the development of improved therapies. - Source: PubMed
Publication date: 2026/03/02
Cronin Joseph MTu Mei-JuanWang YimeiYu Ai-Ming - Cardiac function has been found to be particularly vulnerable to climate change and temperature variability. However, the specific molecular mechanisms underlying the pathogenesis of heat stroke (HS)-induced myocardial dysfunction remain largely elusive. In this study, we constructed a cardiomyocyte-specific peroxisome proliferator-activated receptor γ (PPARγ) knockout mouse model subjected to HS to investigate the key role of PPARγ. RNA sequencing analysis was performed to identify downstream targets of PPARγ. Rosiglitazone, a PPARγ agonist, was examined for its therapeutic potential against HS-induced myocardial injury. Our results showed that HS significantly downregulated the expression of PPARγ. Cardiomyocyte-specific knockout of PPARγ exacerbated myocardial injury in mice subjected to HS. RNA-seq analysis revealed that differentially expressed genes were mainly enriched in lipid metabolism-related pathways, particularly ABC transporters. Further experiments demonstrated that ABCC5 serves as a pivotal downstream factor mediating the cardioprotective effects of PPARγ overexpression against HS. HS also led to the accumulation and deposition of lipids in the myocardium and serum over an extended period, which was partly attributed to the downregulation of the PPARγ/ABCC5 pathway. Importantly, we demonstrated that treatment with either rosiglitazone (a PPARγ agonist) or atorvastatin (a lipid-lowering drug) holds promising therapeutic potential for ameliorating HS-induced myocardial dysfunction. These findings indicate that PPARγ protects against HS-induced myocardial pathological manifestations through ABCC5-dependent regulation of lipid metabolism. - Source: PubMed
Publication date: 2026/03/05
Shen MingzhiZhao AizhenHao GuangzhiLei WangruiLi NingDeng ChaoWang XueChen YingZhang ZheDong YushuYang Yang - Sorafenib is a cornerstone in the treatment of advanced HCC. However, its clinical efficacy is frequently limited by the development of resistance, contributing to unfavorable patient outcomes. Overcoming this resistance is therefore a critical therapeutic challenge. Emerging evidence highlights ferroptosis-a regulated cell death process driven by iron-dependent lipid peroxidation-as a promising avenue to reverse sorafenib resistance. SLC7A11 (cystine/glutamate antiporter) and GPX4 (phospholipid hydroperoxidase) cooperate to maintain redox homeostasis by supporting glutathione biosynthesis and neutralizing lipid peroxides, thereby inhibiting ferroptosis. Nrf2, a master transcriptional regulator of antioxidant responses, further enhances this defense by upregulating both SLC7A11 and GPX4, protecting HCC cells from sorafenib-induced ferroptotic death. In contrast, lipid metabolism remodels membrane phospholipid composition to promote ferroptosis resistance. This review systematically examines the key regulatory axes modulating ferroptosis in this context: the Nrf2/SLC7A11/GPX4 antioxidant axis, the parallel FSP1-CoQ10 pathway, the pro-ferroptotic ACSL4/LPCAT3 axis, and central transcriptional regulators of SLC7A11, including P53, ATF4, SAT1, and ABCC5. We synthesize recent advances linking these molecular axes to ferroptosis pathways, discuss their crosstalk in sorafenib-resistant HCC, and underscore emerging therapeutic strategies that leverage pharmacological or radiotherapeutic targeting of these mechanisms. A deeper understanding of this regulatory network may inform rational combination therapies aimed at resensitizing advanced HCC to sorafenib. - Source: PubMed
Publication date: 2026/02/26
Che LinlinZhu LiujingZhou LingZhou Yufu - DENV virus (DENV) infection can cause various symptoms and organ damage, even severe dengue fever. However, the underlying host response products and interfering metabolic pathways and mechanisms of DENV infection remain unclear. In this study, we characterized the metabolites and metabolic pathway changes during DENV infection using liquid chromatography- (LC-MS) and gas chromatography-mass spectrometry (GC-MS). And identify the hub differentially expressed targets associated with major metabolism pathways combining transcriptomics. - Source: PubMed
Publication date: 2026/02/11
Liu ChengxinYe BeiWang KaiChen JiafangHuang HuitingJiang YongLi GengZhan Shaofeng - Remote ischemic preconditioning (RIPC) is a promising, non-invasive strategy for reduction in ischemic injury after stroke, yet its molecular mechanisms and translatability from animal models to humans remain insufficiently defined. In particular, whether RIPC-induced gene programs causally contribute to reduced stroke risk in humans is unclear. Here, we aimed to establish a translational framework linking RIPC-induced gene regulation in mice to causal genetic and epigenetic determinants of stroke risk in humans. - Source: PubMed
Publication date: 2026/02/13
Liu ShanpengWu QikeWang TingLuo ZhengXu CanLi WanxianZhang RongpingZhu YingHuang ShengLiu CuiyingZhao Heng