Ask about this productRelated genes to: SLC27A5 antibody
- Gene:
- SLC27A5 NIH gene
- Name:
- solute carrier family 27 member 5
- Previous symbol:
- -
- Synonyms:
- FATP5, VLACSR, VLCS-H2, VLCSH2, FACVL3, FLJ22987, ACSVL6, ACSB
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-20
- Date modifiied:
- 2016-02-17
Related products to: SLC27A5 antibody
Related articles to: SLC27A5 antibody
- Hepatocellular carcinoma (HCC) exhibits diminished capacity for oxidative utilization of long-chain fatty acids (LCFAs). However, the strategic and mechanistic basis by which HCC cells enact metabolic reprogramming to adapt to impaired LCFAs oxidation and sustain viability remains incompletely defined. Here we report that solute carrier family 27 member 5 (SLC27A5), the specific transporter for LCFAs, is broadly downregulated in HCC cells, resulting in reduced LCFAs uptake. In HCC cells with impaired LCFAs oxidation, diminished LCFAs import caused by SLC27A5 loss does not lead to energy deficiency, but instead prevents lipotoxicity derived from unutilized LCFAs, thereby supporting HCC cell growth. Impaired LCFAs oxidation suppresses peroxisome proliferator-activated receptor alpha (PPAR-α) signaling, which in turn represses SLC27A5 transcription, accounting for the widespread downregulation of SLC27A5 in HCC. Owing to reduced LCFAs uptake, HCC cells with low SLC27A5 rely on the glutamine reductive pathway for fatty acid biosynthesis to maintain total fatty acid levels, rendering these cells highly sensitive to glutaminase inhibition. In conclusion, we demonstrate that SLC27A5 downregulation represents a response to defective LCFAs oxidation in HCC, and reduced LCFAs uptake consequent to low SLC27A5 expression constitutes a survival adaptation that enables HCC to tolerate impaired LCFAs oxidation. Glutaminase inhibitors may serve as a precision therapeutic strategy for HCC characterized by low SLC27A5 expression. - Source: PubMed
Publication date: 2026/05/26
He XiaoyanZhao ZhengweiWei TengZheng LisiYang JincuiHe XinrongCheng YicaiZhan XiaoyiLi ZejuanWu KelinRoessler StephanieJian YuntingFu ChuliYan Guang-RongXu JunyaoZhang Qiangnu - Hepatic diseases pose a major and life-threatening global health challenge. Sesaminol, a sesame-seed lignan with antioxidant and anti-inflammatory properties, was investigated for its ability to combat metabolic dysfunction-associated fatty liver disease (MAFLD) and alcohol-related liver injury. Mice fed a high-fat diet (HFD) or subjected to binge alcohol injury received oral sesaminol to evaluate its protective effects against hepatic dysfunction. Complementary in vitro studies used HepG2 cells to delineate the potential mechanism. Sesaminol reduced body-weight gain, enhanced glucose tolerance and insulin signaling, lowered hepatic and serum lipid accumulation, and attenuated the inflammatory response in mice. Moreover, sesaminol dose-dependently reduced triglyceride (TG) accumulation and suppressed pro-inflammatory cytokines in vitro. Transcriptomic and docking analyses identified peroxisome proliferator-activated receptor alpha (PPARα) as a direct sesaminol target and revealed solute carrier family 27 member 5 (Slc27a5) as a novel downstream gene. Sesaminol enhanced PPARα occupancy on the Slc27a5 promoter, increased fatty acid uptake, and restored mitochondrial β-oxidation flux. Therefore, sesaminol may function as a natural PPARα agonist that links fatty acid import to mitochondrial oxidation via Slc27a5, thereby ameliorating hepatic steatosis and inflammation in both metabolic and alcohol-related liver dysfunction. - Source: PubMed
Zheng LiujieZhou JunJin HaojieLong YuZheng YifanDing KunyingZheng ZiyiZhuge FenFu ZhengweiNi Yinhua - Advanced glycation end products (AGEs) are significant byproducts of the Maillard reaction and are implicated in degenerative diseases. Catechin (CC), a dietary polyphenol distributed in fruits and vegetables, inhibits AGEs formation through binding with carbonyl compounds. However, the biological role of these binding adducts remains unclear. This study first isolated the major CC-methylglyoxal (MGO) adducts using high-speed counter-current chromatography. Structural analysis confirmed it retains antioxidant phenolic hydroxyls. In food models (lactose/lysine and milk), CC-MGO significantly inhibited AGEs formation, an effect that may be partly attributed to its antioxidant activity. In Caco-2 cells, CC-MGO alleviated AGEs-induced cytotoxicity. Transcriptomics revealed AGEs activated the AGE-RAGE pathway (upregulating CXCL8, CCL2), while CC-MGO counteracted toxicity by modulating PPAR and IL-17 pathways, specifically upregulating SLC27A5 and downregulating MMP1 and PCK1. These findings demonstrate that CC not only scavenges carbonyls but also forms bioactive adducts that further suppress AGEs formation and toxicity, providing a dual mechanism for natural intervention. - Source: PubMed
Publication date: 2026/05/04
Yan JiaZhang XingyuZhao XinruTan JiangyingBao ChenxuZhou ChenHe BoqianLi YinxinLu BaiyiLiu LianliangYi FanWu Qian - Pediatric populations differ from adults in drug elimination capacity. While current scaling methods account for enzyme and transporter maturation, they overlook comorbidities, such as biliary atresia (BA), a liver disease appearing within the first 2-8 weeks of life that can progress to cirrhosis. Such conditions may impair hepatic drug clearance, requiring dose adjustments. Physiologically based pharmacokinetic (PBPK) tools aim to address such cases and have been advocated to fill gaps in clinical data instead of less formalized and evidence-based guesswork. However, the paucity of systems data in rare disease populations has hindered the development of robust PBPK models. This study used global liquid chromatography and tandem mass spectrometry (LC-MS/MS) proteomics to quantify drug-metabolizing enzymes and transporters in diseased neonatal (n = 13) and infant (n = 12) liver samples, revealing significant expression changes in biliary atresia (BA) livers vs. controls (n = 19). Based on cohort means, CYP2A6, CYP2B6, and CYP2E1 levels were 6-17-fold higher in BA livers compared to controls, while CYP4F11 and CYP20A1 were reduced. UGT1A1, UGT2B4, and UGT2B7 showed up to 16-fold higher abundance in neonates with BA. Among transporters, ABCF1 abundance increased dramatically (46-fold), whereas B3AT/SLC4A1, ADT1/SLC25A4, and S27A5/SLC27A5 were decreased. The observed alterations suggest that assuming similar liver function in BA and non-BA patients has implications, with impact varying by drug clearance pathway. While in silico models can explore this, clinical pharmacokinetic studies in BA are essential for verification. To our knowledge, such studies are absent. Our observations underscore the urgent need for dedicated pharmacokinetic studies in BA patients to improve precision dosing. - Source: PubMed
Publication date: 2026/03/04
Al-Majdoub Zubida MHoward MartynAchour BrahimBarber JillAlizai NavedRostami-Hodjegan Amin - N-acyl taurines (NAT) are endogenous, bioactive conjugates of fatty acids and taurine with roles in carbohydrate and lipid metabolism. In the liver, NATs are synthesized by bile acid-CoA:amino acid N-acyltransferase (BAAT), which also conjugates bile acids to taurine or glycine, suggesting an overlapping hepatic synthesis pathway. BAAT catalyzes the transfer of an acyl-chain from an activated coenzyme A (CoA) to taurine, but the hepatic enzyme responsible for synthesizing the acyl-CoA remains unknown. Using liver transcriptomics in mice unable to hydrolyze NATs, we identified Slc27a5, which encodes the acyl-CoA synthetase, fatty acid transport protein 5 (FATP5), as a potential regulator of hepatic NAT synthesis. In vivo knockdown of the enzyme confirmed that FATP5 is necessary for hepatic NAT synthesis and upstream of BAAT, likely through its acyl-CoA synthetase activity. The dual function of this enzyme in activating both fatty acids and bile acids for conjugation identifies a functional overlap between the hepatic NAT and bile acid production pathway. - Source: PubMed
Publication date: 2026/03/02
Kuentzel Katharina BTrammell Samuel A JHassing Anna SGarfinkel Benjamin PBradić IvanTchoukoua KathleenGillum Matthew PLarsen Martin RGrevengoed Trisha J