ABCF1
- Known as:
- ABCF1
- Catalog number:
- 000930A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCF1
Related genes to: ABCF1
- Gene:
- ABCF1 NIH gene
- Name:
- ATP binding cassette subfamily F member 1
- Previous symbol:
- ABC50
- Synonyms:
- EST123147
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-07
- Date modifiied:
- 2015-11-13
Related products to: ABCF1
Related articles to: ABCF1
- Myocardial infarction (MI) is linked to high mortality, which highlights the need for early diagnosis and intervention to prevent heart failure. N6-methyladenosine (m6A) methylation of ribonucleic acid (RNA) influences endothelial dysfunction and MI. Here, the effects and associated mechanisms of fat mass and obesity-associated gene (FTO) on vascular endothelial cell (EC) function, as well as myocardial damage in mice following MI were investigated. - Source: PubMed
Publication date: 2026/06/04
Pan HuichaoXu XunlongYu YameiQiu ZhaohuiZhou Yafeng - Nutritional interventions and bioactive supplements have attracted increasing attention as strategies for managing metabolic dysfunction-associated steatotic liver disease (MASLD). Among them, Forskolin (FSK), a bioactive diterpenoid derived from Coleus forskohlii, is widely used as a dietary supplement for weight management. This study investigated the hepatoprotective effects of FSK and the underlying metabolic mechanisms in MASLD. C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks to induce MASLD and received FSK or metformin (Met). AML12 and Raw264.7 were co-cultured and treated with FSK or phloretin (PHL). FSK reduced lipid droplet accumulation, de novo lipogenesis (DNL), and inflammatory activation in vitro and in vivo, and further attenuated collagen deposition in HFD-fed mice. Notably, FSK decreased the expressions of glucose transporter 1 (GLUT1) and ATP-binding cassette subfamily F member 1 (ABCF1), reduced glycolytic activity and ATP production, and attenuated aberrant nucleocytoplasmic shuttling of hepatocyte nuclear factor 4 alpha (HNF4α) in vitro and in vivo. These effects were abolished by GLUT1 or ABCF1 silencing. FSK also regulated the interactions among GLUT1, ABCF1, and HNF4α. Cellular thermal shift assay (CETSA) and molecular dynamics analysis further supported a potential interaction between FSK and GLUT1. FSK prevented lipid metabolic dysregulation through the GLUT1/ABCF1-HNF4α axis in AML12 induced by M1-polarized macrophages, particularly under oleic acid (OA) co-stimulation. FSK also inhibited inflammatory activation in macrophages induced by IL-1β derived from OA-stimulated AML12. Collectively, these findings support the potential of FSK as a functional dietary supplement for the management of MASLD. - Source: PubMed
Publication date: 2026/05/18
Liu Sai-HuXuan Mei-YanGao ChongZheng ShuangZhang Jia-XinLian Li-HuaNan Ji-XingCui Zhen-YuWu Yan-Ling - Innate immunity constrains the hepatitis B virus (HBV) by sensing pathogen-associated molecular patterns (PAMPs) and inducing type I/III interferons and interferon-stimulated genes. This review synthesizes molecular mechanisms by which HBV nucleic acids and proteins are detected by pattern recognition receptors (PRRs) and how the virus evades such surveillance. At the DNA level, covalently closed circular DNA (cccDNA) persists as a chromatin-like episome with low immunogenicity; cGAS-STING signaling is functionally dampened, whereas nuclear interferon-inducible protein 16(IFI16) and cytoplasmic/nuclear ABCF1 bind cccDNA to repress transcription, and APOBEC3A-mediated deamination requires robust interferon signaling. At the RNA level, TLR3/7/8 and retinoic acid-inducible Gene I(RIG-I) sense circulating HBV RNA and 5'-triphosphate pregenomic RNA, respectively. HBV counteracts RIG-I-like receptor (RLR) pathways through ADAR1 editing, TIAR-dependent translational control, and a metabolic checkpoint involving lactate-MAVS/hexokinase, whereas spliced viral RNAs (svRNAs) have emerged as immunologically relevant species. At the protein level, Hepatitis B Surface Antigen (HBsAg) impairs interferons (IFN) induction by blocking the TAK1-TAB2-NF-κB/IRF axis; Hepatitis B Virus X Protein (HBx) sustains cccDNA transcription via DDB1-directed Smc5/6 degradation and broadly suppresses PRR/IFN signaling, with TRIM25 acting as a host restriction factor. These insights nominate combinatorial strategies-PRR agonists (TLR/STING), MAVS sensitization, metabolic disinhibition, pharmacological disruption of the HBx-DDB1 axis, and reinforcement of IFI16/ABCF1-to achieve functional control of cccDNA and advance curative hepatitis B virus (HBV) therapy. - Source: PubMed
Publication date: 2026/03/03
Chen ZhenghaoHu RuiYe HuajunChen QiuxunLiu YuhangZhang XinyuChen YingtingWu YouJin Ciliang - 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 - Lung adenocarcinoma (LUAD) is the most prevalent histological subtype of lung cancer, and the development of chemoresistance often leads to tumor recurrence and metastasis. Neurotrophic receptor tyrosine kinase 2 (NTRK2) has been implicated in tumorigenesis and chemotherapy resistance, but its precise role in LUAD and contribution to paclitaxel resistance remain unclear. In this study, we found that NTRK2 expression was significantly upregulated in LUADs compared with paired noncancerous tissues and was further elevated in samples from patients who experienced recurrence following paclitaxel-based chemotherapy. Functional assays demonstrated that NTRK2 knockdown markedly inhibited the malignant phenotypes of LUAD cells in vitro and significantly restored the sensitivity of LUAD cells to paclitaxel. Conversely, NTRK2 overexpression promoted cell proliferation, colony formation, and reduced responsiveness to paclitaxel. Consistently, in vivo xenograft experiments revealed that NTRK2 knockdown suppressed tumor growth and enhanced the antitumor efficacy of paclitaxel. Mechanistically, NTRK2 activated the MAPK/ERK and PI3K/AKT signaling pathways, leading to the upregulation of MYC, which in turn directly activated the transcription of ATP-binding cassette subfamily F member 1 (ABCF1), thereby promoting LUAD progression and paclitaxel resistance. Collectively, our findings identify NTRK2 as a critical oncogenic driver that confers chemoresistance by activating the NTRK2/MYC/ABCF1 signaling axis. This study provides new mechanistic insights into the regulation of paclitaxel resistance in LUAD and highlights NTRK2 and its downstream effectors as promising therapeutic targets for overcoming chemoresistance. - Source: PubMed
Publication date: 2026/01/06
Cui RongrongWang YuanyuanYao YaoRen XiaojuanZhang YuchenLi DaxuHou PengJi MeijuQu Yiping