Ask about this productRelated genes to: FABP4 protein
- Gene:
- FABP4 NIH gene
- Name:
- fatty acid binding protein 4
- Previous symbol:
- -
- Synonyms:
- A-FABP, aP2
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-01-18
Related products to: FABP4 protein
Related articles to: FABP4 protein
- Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disease with high heterogeneity and currently lacks approved targeted therapies. Identifying druggable genes with diagnostic relevance and potential translational value may facilitate further research into precision medicine approaches for NAFLD. This study integrated transcriptome data from three independent GEO datasets (GSE33814, GSE63067, and GSE89632) and used sva and limma to correct for batch effects. Differentially expressed genes (DEGs), druggable genes obtained from DGIdb, and genes from WGCNA modules significantly associated with NAFLD were intersected to identify candidate genes. Candidate genes were systematically evaluated using functional enrichment analysis (GO, KEGG, GSEA), immune infiltration analysis (CIBERSORT), receiver operating characteristic (ROC) analysis, and co-expression networks. Finally, the expression of key genes was verified by immunohistochemistry (IHC) and immunofluorescence (IF). A total of nine key candidate drug targets were identified: FABP4, ADAMTS1, FOS, GPR88, IL1RL1, CD52, JUN, SERPINE1, and THBS1. These genes are primarily involved in metabolism, inflammatory response, extracellular matrix remodeling, and immune regulation. ROC analysis showed that FOS and JUN had high diagnostic accuracy. Furthermore, IHC and IF results demonstrated that CD52 was significantly upregulated in NAFLD tissues, suggesting its potential relevance as a candidate target for further investigation. This study systematically identified key druggable genes for NAFLD through bioinformatics analysis and partially validated selected candidates experimentally. In particular, CD52 was upregulated in NAFLD tissues, suggesting a potential association with NAFLD-related pathological alterations. These findings provide new insights into the molecular pathogenesis of NAFLD and may provide a basis for future target validation studies. - Source: PubMed
Publication date: 2026/05/20
Zhang XiangqianSu HanyangZhou QuanZhou Yuling - Intramuscular fat (IMF) plays an important role in determining meat quality traits such as flavor, tenderness, and juiciness. While numerous studies have investigated the genetic basis of IMF in commercial pig breeds, data on local breeds remain rather limited. In this study, we used RNA-sequencing to characterize the transcriptomic differences between high-IMF and low-IMF Black Slavonian pigs, a native Croatian breed known for superior meat quality. Muscle samples (Longissimus thoracis et lumborum) from 14 pigs with divergent IMF levels were collected shortly after slaughter, preserved in liquid nitrogen, and stored at - 80 °C until RNA extraction. Intramuscular fat content was determined from the same muscle 24 h post mortem using the Soxhlet extraction method (ISO 1443:1973). These samples were then analyzed to identify differentially expressed genes (DEGs) and enriched pathways. A total of 519 genes were differentially expressed (p ≤ 0.05), with 457 remaining significant after false discovery rate correction. The high-IMF group exhibited upregulation of genes associated with lipid metabolism (e.g., SCD, ADIPOQ, CIDEC, FABP4), PPAR signaling, and adipogenesis, while genes linked to muscle structure and oxidative metabolism were downregulated. Functional enrichment and gene set enrichment analyses highlighted coordinated regulation of pathways related to fatty acid biosynthesis, extracellular matrix (ECM) remodelling, angiogenesis, and Notch signaling. Notably, several ECM-related genes (LAMA1, TIMP4) and angiogenic factors (FGF2, NRP1) were significantly upregulated, suggesting that adipocyte expansion in muscle requires parallel vascular and structural adaptations. Importantly, several of the top 30 DEGs, including EHD2, NRG4, UTRN, FLNA, and HMCN1, represent novel candidate genes not previously linked to IMF in pigs, pointing to potential breed-specific mechanisms. These genes are associated with membrane trafficking, paracrine signalling, cytoskeletal re-modelling, and ECM dynamics. Our findings contribute new molecular insights into IMF regulation in local pig breeds and provide a foundation for developing targeted breeding strategies to improve pork quality through intramuscular fat enhancement. - Source: PubMed
Publication date: 2026/05/20
Lukic BorisLipavić GoranBulaić MatejaIno CurikRadišić ŽarkoLužaić RasRaguž Nikola - Colorectal cancer (CRC), a lethal tumor of the intestine, has lipotoxicity, which exerts a significant influence on the onset and development of intestinal disorders. This study provides an in-depth evaluation of lipotoxicity-related genes (LRGs) in the CRC treatment setting. - Source: PubMed
Publication date: 2026/05/20
Xiong ChenluLiao PinglianLi Jin - MicroRNAs (miRNAs) play central roles in cancer pathogenesis by modulating oncogenic and tumor-suppressive pathways. The microRNA-29 (miR-29) family, known to inhibit matrix metalloproteinase-2 (MMP-2), represents a key regulatory axis in tumor invasion. This study analyzed miRNA pathway enrichment derived from tumor-normal mRNA differential expression in esophageal squamous cell carcinoma (ESCC) patients and investigated whether Ilomastat, a known MMP inhibitor, could plausibly bind the catalytic site of MMP-2. Thirty-eight patients with suspected esophageal cancer were recruited from an Academic Hospital in 2024. Twenty-nine ESCC patients were finally included. Paired tumor/adjacent-normal tissues were collected using endoscopic biopsies. Total RNA was extracted, sequenced, and bioinformatics conducted using the nf-core/rnaseq pipeline, with pathway enrichment analysis completed using g:Profiler2. Additional computational docking studies were performed to assess whether Ilomastat tautomers could plausibly bind the catalytic site of MMP-2. Pathway enrichment analysis identified several miRNAs implicated in ESCC pathogenesis, including the miR-29 family. Transcriptome analysis revealed overexpression of LINC00392 and FABP4 (fatty acid-binding protein 4) among the differentially expressed genes. FABP4 drives lipid metabolic reprogramming and tumor microenvironments that support cancer cell proliferation and metastatic potential. Computational docking suggested that the neutral tautomer of Ilomastat favorably occupies the catalytic site of MMP-2, providing a hypothesis-generating structural rationale for downstream pharmacologic inhibition of MMP-2. This study integrates pathway-based miRNA enrichment and computational docking to highlight the miR-29-MMP-2 axis as a potential regulatory pathway in ESCC. Collectively, our findings provide hypothesis-generating support for miRNA-guided MMP-2 inhibitor design that bridges transcriptomic discovery with pharmacologic modeling. - Source: PubMed
Publication date: 2026/05/18
Mbatha Sikhumbuzo ZAlaouna MohammedDamane BotleMarutha TebogoDakurah Ottovon BDlamini Zodwa - Estrogens are global regulators of cellular signaling pathways, impacting fundamental processes and phenotypes that are essential for tissue remodeling and homeostasis. Traditional cell culture media contains estrogen-mimetic compounds, including phenol red and endogenous estrogen in fetal bovine serum (FBS). However, the potential of these compounds to bias in vitro studies, particularly when considering sex as a biological variable, remains unclear. This gap in understanding critically impacts the culture of human mesenchymal stromal cells (hMSCs), whose basic functions and differentiation potential, central to cell therapy and tissue engineering, are sensitive to perturbations in the culture conditions. Despite this, the effect of estrogens from cell culture media on male and female hMSCs is not currently considered in cell processing for clinical trials. As such, a baseline understanding of these estrogen-mimetic media influences on hMSCs is critical for clinical efficacy and adequate study design in research. To this end, we investigated the effects of phenol red and fetal bovine serum on the proliferation, metabolism, senescence, and differentiation capacity of male and female hMSCs. Phenol red, FBS, donor sex, and 17β-estradiol (E2) supplementation all had significant impacts on hMSC health and differentiation potential in culture. Notably, dosing with estrogen at the levels found in FBS did not recover most of the hMSC metrics tested. The notable outcomes that were significantly impacted by sex for the overall analysis include proliferation, metabolism, senescence, osteogenic differentiation, adipogenic differentiation, and gene expression for Col1a1, ESR1, Col10a1, RUNX2, FABP4, and PPARγ. Donor variability was a main driver in all the outcomes tested, highlighting the need for personalized medicine in research investigating cellular response to hormone signaling. Overall, these findings reveal the sex-biased effects of estrogen and estrogen-mimetic compounds in traditional culture media, underscoring a current gap in considering sex as a biological variable in cell therapy and tissue engineering research and manufacturing. - Source: PubMed
Publication date: 2026/05/19
Bradford John CRobinson Jennifer L