Ask about this productRelated genes to: Lgals4 Blocking Peptide
- Gene:
- LGALS4 NIH gene
- Name:
- galectin 4
- Previous symbol:
- -
- Synonyms:
- GAL4
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-24
- Date modifiied:
- 2016-05-13
Related products to: Lgals4 Blocking Peptide
Related articles to: Lgals4 Blocking Peptide
- Lectin-glycosaminoglycan (GAG) interactions remain incompletely understood despite their potential roles in cell signaling and immune regulation. In this study, we performed a comprehensive profiling of the binding specificity of 49 types of human endogenous lectins-including SIGLECs, C-type lectins, and galectins-for GAGs using GAG microarrays. GAGs containing 6-O-sulfation, such as heparin (HP), chondroitin sulfate C (CSC), and chondroitin sulfate E (CSE), exhibited broad binding to multiple SIGLECs and C-type lectins, whereas non-sulfated or low-sulfated GAGs exhibited minimal interactions, indicating a strong dependence on sulfation patterns. In contrast, most galectins displayed little or no detectable binding to GAG. Notably, galectin-4 (Gal-4) uniquely exhibited significant affinity for 6-O-sulfated GAGs, particularly HP. Surface plasmon resonance analysis revealed high-affinity binding of Gal-4 to HP (Kd = 4.70 × 10 M), substantially stronger than its carbohydrate recognition domains, indicating cooperative contributions of both N- and C-terminal CRDs of Gal-4. Molecular dynamics simulations further supported a binding mode involving both N- and C-terminal domains. Consistent with these findings, Gal-4 bound to endogenous HP-positive mast cells, and this interaction was competitively inhibited by HP. Together, these results identify Gal-4 as a unique galectin with a noncanonical capacity to recognize sulfated GAGs, revealing an alternative glycan-recognition mechanism beyond the conventional β-galactoside paradigm. - Source: PubMed
Publication date: 2026/06/29
Sano KanaeNagatomo MeriShigematsu KatsunobuYamasaki KazuhikoAnh Dinh Xuan TuanShibuya AkiraOtsuka YuyaMinamisawa ToshikazuTateno Hiroaki - Prostate cancer (PC) progression and mortality are largely driven by therapeutic resistance, increasingly linked to dynamic tumor-stroma interactions. However, the molecular basis of cancer-fibroblast crosstalk remains incompletely understood, particularly the contribution of Interleukin (IL)-30, an emerging regulator of PC aggressiveness. Here, we demonstrate that IL30 produced by PC cells reprograms stromal fibroblasts via IL6Rα/gp130 signaling, activating AKT and TGF-β/BMP pathways to drive their proliferation and differentiation into pro-angiogenic cancer-associated fibroblasts (CAFs). Reciprocally, these fibroblasts amplify IL30-mediated tumor aggressiveness by enhancing oncogenic transcriptional programs and by promoting cancer cell migration. Notably, while fibroblast co-culture suppresses epithelial-mesenchymal transition (EMT)-associated genes in PC cells, including NOTCH1, SNAI1/2 and ZEB1, IL30 overexpression overrides this effect, inducing EMT regulators alongside key PC-associated genes, such as IL6, LGALS4, HAL, and SHBG, whose expression correlates with IL30 levels in clinical bone metastasis datasets. Using a two-organ-on-chip platform linking PC-fibroblast spheroids to a bone marrow-like niche, we show that fibroblasts enhance PC cell migration and colonization of the bone marrow microenvironment, effects potentiated by IL30 overexpression and largely abrogated by its genetic depletion. Collectively, these findings identify an IL30-driven tumor-stroma signaling axis that promotes microenvironmental remodeling and metastatic progression, highlighting a potential therapeutic target to counteract PC progression and treatment resistance. - Source: PubMed
Publication date: 2026/06/24
Ciummo Stefania LiviaSorrentino CarloMarchetti SimonaFieni CristianoLanuti PaolaDi Carlo Emma - This study investigates the inhibitory effect of astragaloside II (AGS-II) on colorectal cancer (CRC) progression and elucidates the underlying mechanism involving LGALS4. The effects of AGS-II on proliferation, migration, and apoptosis of CRC cells were assessed using cell counting kit-8, colony formation, scratch wound, and flow cytometry assays. Potential targets were screened through integrated bioinformatics analysis and validated via RT-qPCR and Western blot. Molecular docking and molecular dynamics simulation were performed to evaluate the direct interaction between AGS-II and LGALS4. Functional experiments were conducted using gene overexpression and RNA interference. An in vivo xenograft model was employed to assess therapeutic efficacy. AGS-II significantly inhibited CRC cell proliferation and migration while inducing apoptosis in a dose-dependent manner. Bioinformatics analysis and experimental validation identified LGALS4 as a key target of AGS-II, with its high expression correlating with favorable patient prognosis. Molecular docking revealed a favorable binding affinity (Vina score: -9.2 kcal/mol), and molecular dynamics simulation confirmed the stability of the AGS-II-LGALS4 complex over 100 ns. Functional assays demonstrated that LGALS4 overexpression suppressed malignant phenotypes, whereas LGALS4 knockdown reversed the antitumor effects of AGS-II. In vivo experiments confirmed that AGS-II inhibited tumor growth by upregulating LGALS4. AGS-II suppresses CRC progression by upregulating LGALS4 expression, providing a novel candidate target and therapeutic strategy for CRC. - Source: PubMed
Publication date: 2026/06/29
Su YingyingLu DanZhang RongqiangShao Zhiyong - Age-related macular degeneration (AMD) and cardiovascular disease (CVD) share numerous risk factors; however, protein biomarkers for AMD are lacking. We investigated whether circulating cardiovascular peptide biomarkers are associated with AMD in the population-based Białystok PLUS cohort. This cross-sectional analysis included 699 participants aged ≥ 50 years (AMD + = 93; AMD⁻ = 606) examined between 2018 and 2023. AMD was graded from fundus photos with the use of the Wisconsin and modified International Classification systems. Ninety-two cardiovascular proteins were quantified in serum with the Olink Target Cardiovascular III panel. Age-adjusted linear or logistic regressions assessed biomarker-AMD associations, and receiver-operating-characteristic (ROC) curves evaluated discriminative performance. After adjustment, AMD+ participants exhibited lower galectin-4 (β = - 0.15, p = 0.043) and TNF-receptor-superfamily-member-10 C (TNFRSF10C) (β = - 0.17, p = 0.037) concentrations and higher von Willebrand factor (vWF) levels (β = 0.22, p = 0.036) versus AMD⁻ individuals. Galectin-4, TNFRSF10C, and vWF predicted AMD with areas under the ROC curve of 0.613 (95% confidence interval [CI] 0.516-0.709), 0.606 (0.520-0.692), and 0.594 (0.500-0.687), respectively. Optimal cut-offs were 4.05 NPX for galectin-4, 5.09 NPX for TNFRSF10C, and 8.03 NPX for vWF, yielding sensitivities/specificities of 57%/63%, 58%/62% and 55%/63%, respectively. Elevated vWF and reduced galectin-4 and TNFRSF10C are independently associated with AMD, suggesting overlapping vascular, inflammatory and apoptotic pathways with CVD. Incorporation of these peptides into risk-stratification algorithms could enhance early AMD detection and motivate mechanistic studies targeting the TRAIL-TNFRSF10C axis and galectin-mediated signaling. - Source: PubMed
Publication date: 2026/06/17
Budnik AgnieszkaTuchliński JakubLisowski ŁukaszMichnowska-Kobylińska MagdalenaDmuchowska Diana AnnaChlabicz MałgorzataSzpakowicz AnnaDubatówka MarlenaKondraciuk MarcinKamiński KarolKonopińska Joanna - Although insomnia is associated with increased mortality in patients with depression, the underlying biological pathways remain unclear. As functional gene products, proteins are well suited to bridge behavioural risk factors and clinical outcomes. - Source: PubMed
Publication date: 2026/06/13
Liu XuesongXu HongliZhu XiaoqianTu JiabinLin KaiyangGuo Yansong