Ask about this productRelated genes to: SLC27A5 Blocking Peptide
- 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 Blocking Peptide
Related articles to: SLC27A5 Blocking Peptide
- 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 - Ochratoxin A (OTA), a common food-borne mycotoxin, is a potential human carcinogen, yet the specific molecular mechanisms linking it to hepatocellular carcinoma (HCC) remain unclear. - Source: PubMed
Publication date: 2026/01/28
Zhuo JunyiWu HuaZhou XiaolingWang XiQiu TianqiLin MinTang Yu - To construct gene knockout mice and investigate changed conditions in the serum lipidomics. Liver tissues and serum samples were collected from wild-type and Slc27a5 gene knockout mice at different time points. Hematoxylin-eosin staining was used to observe hepatic pathological changes. Immunofluorescence staining was used to detect the expression of α-smooth muscle actin and F4/80 proteins. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to analyze changes in serum lipid composition. The comparison of quantitative data was performed using the t-test between groups. The percentage area of α-smooth muscle actin staining (7.33% ± 3.08% . 1.14% ± 0.30%, =3.996, <0.01) and F4/80 staining area (2.48% ± 0.71% . 0.76% ± 0.19%, =4.683, <0.01) was significantly higher in gene-deficient mice than in wild-type mice in liver tissue at 24 months of age. The results of the serum lipidomics analysis indicated significant alterations in lipid composition of gene-deficient mice. Compared with wild-type mice, the serum of gene-deficient mice had increased levels of 19 types of phosphatidylinositols and 14 types of phosphatidylcholines and decreased levels of 17 types of phosphatidylethanolamines. Spontaneous liver fibrosis induced by deficiency in a mouse model is accompanied by significant remodeling of the serum lipid profiles. - Source: PubMed
Zheng J HWu KWang KTang N - This study aims to investigate the optimal dose ratio and mechanisms of the primary active components in Yinchenhao decoction (geniposide, chlorogenic acid, and rhubarb polysaccharides) for ameliorating metabolic-associated steatotic liver disease (MASLD). - Source: PubMed
Publication date: 2025/11/19
Gao YanyanXue RuyunXu FangyingChen LinQiu JiannanDou Xiaobing