Ask about this productRelated genes to: MFAP4 antibody
- Gene:
- MFAP4 NIH gene
- Name:
- microfibril associated protein 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-17
- Date modifiied:
- 2017-05-16
Related products to: MFAP4 antibody
Related articles to: MFAP4 antibody
- - Source: PubMed
Publication date: 2026/04/20
Zhang WenxinDai LiangliangLuo MingzhiShi Honglei - Bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH) is a widely used novel flame retardant and an emerging ubiquitous environmental contaminant. While acute exposure disrupts lipid signaling, the long-term consequences of TBPH exposure on the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) remain poorly understood. This study aimed to elucidate the chronic hepatotoxic effects of TBPH and the underlying molecular mechanisms. Adult zebrafish were exposed to environmentally relevant concentrations of TBPH for 6 weeks. Hepatic damage was assessed using histological examination, biochemical assays, and integrated proteomic and transcriptomic profiling. In vitro assays using HepG2 cells were conducted to validate cellular mechanisms of lipid droplet (LD) dynamics. Chronic TBPH exposure induced severe macrovesicular steatosis and significant hepatic fibrosis in zebrafish. Transcriptional analysis revealed that TBPH activated both lipid synthesis and fatty acid oxidation. In vitro results confirmed that TBPH stimulated DGAT2-mediated triglyceride synthesis and promoted LD expansion via ER-LD co-localization. Proteomic analysis identified a microfibril-associated protein 4 (Mfap4) associated with extracellular matrix remodeling and fibrosis. These findings demonstrate that chronic TBPH exposure acts as a potent metabolic disruptor, driving a pathological cascade from steatosis to fibrosis. This study provides a comprehensive adverse outcome pathway for TBPH-induced hepatotoxicity, highlighting its potential role in the etiology of metabolic dysfunction-associated steatohepatitis. - Source: PubMed
Publication date: 2026/03/13
Liu YimingPan DingxiLi MingyingGuo Wei - Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer, accounting for 80% of lung cancer types, with a high metastasis rate and mortality. Here, this experiment investigated the effects of MFAP4 in NSCLC and its molecular mechanisms of ferroptosis in NSCLC. Patients with NSCLC and normal volunteer were obtained from our hospital. The mRNA and protein expression levels of MFAP4 were upregulated in a mouse model of NSCLC. MFAP4 expression levels in cancer cells of NSCLC model through Single Cell Analysis. Sh-MFAP4 reduced cancer growth, and increased Mitochondrial oxidation-induced ferroptosis in mice model of cancer. MFAP4 promoted cell growth, and reduced Mitochondrial oxidation of NSCLC. Si-MFAP4 increased Mitochondrial oxidation of NSCLC. MFAP4 induced FAK expression of NSCLC through the inhibition of FAK Ubiquitination. The m6A/METTL3 modifies MFAP4 expression stability in model of NSCLC by YTHDF1. In conclusion, MFAP4 induced FAK expression to reduce Mitochondrial oxidation-induced ferroptosis of NSCLC model through the inhibition of FAK Ubiquitination. Targeting MFAP4 is thus a potentially effective therapeutic strategy for patients with NSCLC or other cancer. - Source: PubMed
Publication date: 2026/03/08
Li XiaofengXu ChunweiMin YonghuaZhu YoucaiZhai Zhanqiang - Triple-negative breast cancers (TNBCs) are among the most aggressive breast tumors, due not only to the absence of clinically functional biomarkers used in other molecular subtypes, but also their marked heterogeneity and pronounced migratory and invasive behavior. The search for new molecules of interest for risk prediction, diagnosis and therapy stems from the class of long non-coding RNAs (lncRNAs), which often display context-dependent ("dual") functions and tissue specificity. Among them, lncRNA LINC01133 stands out for its dysregulation across cancer, although its molecular role in TNBC remains unclear. In the present study, we used the human TNBC cell line Hs578T to generate a cell panel comprising the parental line (Hs578T_wt), the control line (Hs578T_ctr), and the LINC01133 knockout line (Hs578T_ko). Subsequently, we performed bulk RNA-Seq to identify KO-associated Differentially Expressed Genes (DEGs) using as the primary contrast. Functional interpretation was achieved by Over-Representation Analysis (ORA) using Gene Ontology. We then conducted a comparative patient-cohort analysis using TCGA-BRCA Basal-like/TNBC cases (TCGA/BRCA n = 1098; Basal-like/TNBC n = 199), classified with the AIMS algorithm, and evaluated concordance between KO-associated signatures and patient tumor expression patterns via trend-based analyses across the LINC01133 expression levels and associated genes. A total of 265 KO-dominant DEGs were identified in Hs578T_ko, reflecting transcriptional changes consistent with tumor progression, with enrichment of pathways associated with LINC01133 knockout including cell adhesion, cell-cell interactions, epithelial-mesenchymal transition (EMT), and extracellular matrix (ECM) remodeling. The main DEGs included , , , , , , , , , and with additional candidates, such as and the lncRNA gene , which have been implicated in migration/invasion, ECM remodeling, or signaling across multiple tumor contexts. Translational analyses in TCGA-BRCA basal-like tumors suggested a descriptive association in which lower LINC01133 levels were accompanied by shifts in the expression trends of genes linked to ECM/EMT programs and modulation of genes related to cell adhesion and protease inhibition. : These results suggest a transcriptional model in which LINC01133 is associated with TNBC-related gene expression programs in a concentration-dependent manner, with loss of LINC01133 being associated with a transcriptomic shift toward pro-migratory/ECM remodeling signatures. While functional validation is required to establish causality, these data support LINC01133 as a molecule of interest in breast cancer research. - Source: PubMed
Publication date: 2026/01/24
Teodoro Júnior LeandroJesus-Ferreira Henrique César deSogayar Mari CleideNishiyama-Jr Milton Yutaka - Cardiac fibrosis post-myocardial infarction (MI) induces adverse cardiac remodeling, ultimately resulting in heart failure. Exosomes (EXOs) derived from mesenchymal stem cells (MSCs) have emerged as potent modulators of post-infarction remodeling, capable of limiting fibrotic responses. Our previous study showed that growth differentiation factor 15 as pretreatment promoted the protective effects of MSCs against myocardial fibrosis post-MI via paracrine actions. We investigated whether exosomes derived from GDF15-treated iPSC-MSCs (GDF15-iPSC-MSC-EXOs) could alleviate post-MI fibrosis and further explored the mechanistic pathways underlying their effects. In a mouse model of MI, EXOs released from iPSC-MSCs and GDF15-treated iPSC-MSCs were collected from culture supernatants and subsequently administered intramuscularly around the infarct area. Cardiac fibrosis was assessed by Masson's trichrome staining. A collagen synthesis model in mouse cardiac fibroblasts (mCFs) was established by transforming growth factor-β1 (TGF-β1) treatment in vitro. The mitochondrial morphology of mCFs under TGF-β1 stimulation was evaluated by Mitotracker staining. Delivery of EXOs from GDF15-treated iPSC-MSCs resulted in less fibrotic remodeling and better ventricular function after MI than exosomes from untreated cells. In TGF-β1-stimulated fibroblasts, both exosome types reduced fibrosis markers by preventing mitochondrial fission, with GDF15-iPSC-MSC-EXOs affording stronger protection. These effects were partly attenuated in the presence of the mitochondrial fission activator FCCP. Mechanistically, GDF15, which is rich in GDF15-iPSC-MSC-EXOs, inhibited TGF-β1-induced mCF activation via repression of the MFAP4/ERK/Drp1 pathway through a direct physical interaction with MFAP4. GDF15 conditioning strengthened the capacity of iPSC-MSC-derived exosomes to mitigate cardiac fibrosis following MI via inhibition of mitochondrial fragmentation in CFs by repressing the MFAP4/ERK/Drp1 pathway. GDF15 pretreatment is a novel strategy to enhance the cardioprotection of iPSC-MSC-EXOs against cardiac fibrosis post-MI. - Source: PubMed
Qiu JieHan QianShen YingYang QiLi ZiqiHong YimeiZhao JunxiuLin FangMa KexinHu BeiLiang XiaotingZhang Yuelin