Ask about this productRelated genes to: FGL1 Blocking Peptide
- Gene:
- FGL1 NIH gene
- Name:
- fibrinogen like 1
- Previous symbol:
- -
- Synonyms:
- HFREP-1
- Chromosome:
- 8p22
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-25
- Date modifiied:
- 2015-11-09
Related products to: FGL1 Blocking Peptide
Related articles to: FGL1 Blocking Peptide
- Amphibians face threats from emerging bacterial, viral, and fungal pathogens, and their innate immune response plays a key role in early defense. The liver is a central immune organ that produces acute-phase proteins (APPs) and complement system proteins, which are essential for early pathogen neutralization and a positive disease outcome. Here, we investigated the temporal dynamics of hepatic gene expression for APPs [C-reactive protein (CRP), serum amyloid A (SAA), fibrinogen-like protein 1 (FGL1)] and complement components (C1s, C3, C4, C5, C9) in Rhinella diptycha toads injected with lipopolysaccharide (LPS) or saline. Using RT-qPCR at four time points post-injection (1h, 3h, 6h, and 18h), we detected a significant effect of LPS on C1s expression and a treatment x time interaction for C4, C5, and C9, indicating time-dependent activation of different complement proteins. In contrast, we found no evidence for LPS-induced changes in APPs expression. However, several APPs were positively correlated with complement components, suggesting coordinated regulation even in the absence of differential expression. Our findings provide a temporal analysis of hepatic acute-phase responses to LPS in Rhinella diptycha toads, unraveling a complex network of complement system activation. By showing that complement components, rather than APPs, dominate the early hepatic response to a bacterial antigen in a widespread Neotropical toad species, our study provides a temporal and mechanistic baseline for future investigations of amphibian innate immunity and underscores the need for future work to determine how these early pathways respond to different pathogens and contribute to variation in disease outcomes among amphibians. - Source: PubMed
Publication date: 2026/05/07
Zenga-Carrenho MarinaTiton BrazTiton Stefanny Christie Monteirode Assis Vania ReginaGomes Fernando RibeiroFloreste Felipe Rangel - Immunotherapy has emerged as a first-line treatment for patients with advanced non-small cell lung cancer (NSCLC), but over half of patients fail to benefit, largely due to tumor heterogeneity and a complex tumor microenvironment. Here, we demonstrate that fibrinogen-like protein 1 (FGL1), a recently identified immune checkpoint ligand, is targeted by tripartite motif-containing protein 21 (TRIM21) for proteasomal degradation, thereby enhancing the anti-tumor activity of cytotoxic T lymphocytes (CTLs). We further show that interferon regulatory factor 1 (IRF1) regulates TRIM21 transcription. Artemisinin upregulates the IRF1-TRIM21 axis, promoting FGL1 degradation. In high FGL1 expressed tumors, artemisinin in combination with anti-programmed cell death protein 1 (anti-PD-1) therapy enhances immunotherapeutic efficacy. Clinically, an elevated FGL1/TRIM21 protein ratio is associated with poor prognosis in NSCLC. Collectively, these findings elucidate a post-translational regulatory mechanism of FGL1 in tumor progression and support the development of a rational combination immunotherapy strategy for NSCLC treatment. - Source: PubMed
Publication date: 2026/04/22
Zhang YuchenZhou PingjingGuo YifanZhang HongyuZhao GuangyinYin JunGe DiLiu RonghuaGu JieZhang Chunyi - Metabolic stress results in the production of circulating hepatokines that can be coupled to hepatic injury and vascular dysfunction, but the underlying biochemical signaling routes remain incompletely defined. Hepassocin (HPS; FGL1) is a hepatocyte-derived factor implicated in metabolic inflammation; however, whether it directly programs endothelial pro-atherogenic signaling is unclear. Here, we report that a high-fat diet (HFD) increases serum HPS and that palmitate induces oxidative stress-dependent HPS expression and release from hepatocytes, as these responses are reversed by N-acetylcysteine (NAC). Recombinant HPS directly drives endothelial injury and activation in human umbilical vein endothelial cells (HUVECs), increasing ROS levels and lipid peroxidation (MDA/HO), promoting apoptosis, and enhancing adhesion molecule expression and monocyte-endothelial adhesion. Mechanistically, HPS activates EGFR and engages a redox-amplifying EGFR-NOX1 module characterized by the induction of NOX1 and p22phox, leading to robust oxidative stress signaling. EGFR or NOX1 silencing abolishes HPS-induced redox stress and atherogenic endothelial phenotypes. In parallel, HPS activates p38 downstream of EGFR, and p38 suppression mitigates HPS-driven endothelial activation and monocyte adhesion independent of ROS amplification, revealing a second mechanism. Together, these data define dual, targetable pathways-HPS-EGFR-NOX1/ROS and HPS-EGFR-p38-that mechanistically connect a liver-derived circulating factor to endothelial dysfunction and immune cell recruitment, positioning HPS-EGFR signaling as a tractable axis for metabolic stress-associated vascular disease. - Source: PubMed
Publication date: 2026/04/10
Pyo Min KyungPark Hyung SubKo Jun HwiLim Do SuGwon Hyeon JiAbd El-Aty A MYağan RidvanSong Jin-HoShin Yong KyooJeong Ji HoonJung Tae Woo - Fibrinogen-like protein 1 (FGL1) is a hepatokine that regulates hepcidin through antagonism of the bone morphogenetic protein (BMP) pathway. Although preclinical studies suggest a role for FGL1 in iron metabolism, its clinical behavior in human iron deficiency anemia (IDA) remains unclear. This study evaluates circulating FGL1 levels in IDA and examines its diagnostic performance and relationship with hematologic and biochemical markers. - Source: PubMed
Publication date: 2026/03/06
Saboor MuhammadAbdul Rahim RaghadNabi Dad ShamsahYusuf Abeer MohamedNasser Mshael MohammedMansoor Hayat MohsenGuella AdnaneAlkhayyal Noura - Fibrinogen-like protein 1 (FGL1) has been recently identified as an emerging novel checkpoint ligand of lymphocyte activation gene-3 (LAG-3) with important immunoregulatory functions. In addition to LAG-3, FGL1 also interacts with bone morphogenetic protein 6 (BMP6), activin receptor-like kinase 5 (ALK5) and other unidentified receptors to perform biological functions. Physiologically, FGL1 restrains intrahepatic immunity and preserves tolerance. Pathologically, FGL1 is frequently upregulated in various tumors and autoimmune diseases and is closely related to the occurrence and development of these diseases. Targeting FGL1 has shown preclinical efficacy in enhancing immunotherapy involving programmed death ligand 1 (PD-L1)/PD-1 checkpoint blockade, inhibiting liver metastasis and relieving autoimmunity without overt hepatotoxicity. In this review, we summarize recent advances in FGL1, focus on the immunoregulatory functions of FGL1, and evaluate its potential as a therapeutic target for immune-related diseases. - Source: PubMed
Publication date: 2026/02/18
Xi FengjiaLiu Rongzeng