Ask about this productRelated genes to: Abcf1 antibody
- 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 antibody
Related articles to: Abcf1 antibody
- 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 - Porcine reproductive and respiratory syndrome virus (PRRSV) is a major swine pathogen that causes significant economic losses worldwide. The nucleocapsid (N) protein, the most abundant viral protein in infected cells, plays roles beyond its structural function, influencing various host cellular processes. Here, we report the identification of 301 cellular protein candidates interacting with PRRSV N using EGFP immunoprecipitation combined with label-free quantitative mass spectrometry. The analysis underscores the versatile nature of the N protein in targeting a wide range of cellular proteins and processes across multiple subcellular compartments. We observed strong enrichment of ribosomal proteins, nucleolar proteins involved in ribosome biogenesis, splicing factors, RNA helicases, and DNA-binding proteins involved in chromatin remodeling and DNA damage response. Additionally, we identified proteins involved in viral RNA sensing and intrinsic antiviral mechanisms that may contribute to the immunosuppressive properties of the viral protein. Several interactions were validated and further characterized for RNA dependence, including MYBBP1A, NCL, IGF2BP1, UPF3B, G3BP1, EIF2S1, RFC4, ABCF1, PPM1G, NSUN2, and NOP2. Notably, RTCB and MYBBP1A were identified as host dependency factors for PRRSV infection. Our findings expand the current understanding of PRRSV-host interactions and reveal novel N-interacting proteins that may contribute to viral pathogenesis and immune evasion. - Source: PubMed
Publication date: 2025/09/25
Kovanich DuangnapaKetsuwan KunjimasHengphasatporn KowitThepparit ChutimaSittipaisankul PotchamanWongkongkathep PiriyaSirisereewan ChaitawatTechakriengkrai NavaponNedumpun TeerawutShigeta YasuteruPisitkun TrairakSuradhat Sanipa - Emerging evidence suggests a link between environmental pollution and epigenetic alterations, prompting the need for comprehensive investigations into the relationship between pollutants and health conditions in human populations. This study investigates the interplay between obesity and exposure to toxic metals, examining clinical, serum metal concentrations, and epigenetic signatures. Our approach included serum metal concentration analysis by inductively coupled plasma mass spectrometry and epigenetic analysis using 450k Illumina BeadChips data. Singular value decomposition and linear regression models were used to identify metal associations with DNA methylation. Marked differences were evident in weight, body mass index, glycaemia, High Density Lipoprotein cholesterol (HDL-c), and triglycerides between patients with obesity and without obesity. Metal serum concentrations revealed higher arsenic levels in participants with obesity, while elevated mercury concentrations were found in individuals without obesity. Epigenetic analysis identified 2045 arsenic-associated differentially methylated positions (DMPs) in individuals with obesity, including 57 hypermethylated and 159 hypomethylated sites in promoter regions. These DMPs demonstrated direct associations of arsenic exposure, and traits such as insufficient sleep, smoking, and diseases such as gestational diabetes. Functional enrichment analysis (using traits, gene ontology, and KEGG pathways) highlighted pathways linking obesity and arsenic exposure, specifically the Wnt and TNF signalling pathways. Additionally, hypermethylated sites were linked with cancer, rheumatoid arthritis, and gestational diabetes, emphasizing the intricate relationship between these conditions. Notably, and showed significant differences in methylation associated with arsenic and obesity. The findings provide valuable insights into unravelling the connections between obesity and arsenic exposure, contributing to understand the potential molecular mechanisms and pathways in these intersecting fields. - Source: PubMed
Publication date: 2025/06/13
Noronha Natália YumiRodrigues Guilherme da SilvaWatanabe Lígia MoriguchiNoma Isabella Harumi YoneharaCazier Jean-BaptisteSae-Lee ChanachaiChitta PitaksinPereira Vanessa Aparecida BatistaPinhel Marcela Augusta de SouzaDiani Luísa MariaBarbosa FernandoPlösch TorstenNonino Carla Barbosa