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Demonstrate that galectin-3 plays a critical role in hensin ECM assembly by oligomerizing secreted monomeric hensin.
Our results showed that serum Gal-3 and Gal-9 should not be considered biomarkers of inflammatory bowel disease. Despite not being a specific marker for Crohn's Disease, serum Gal-3BP might be used as an adjuvant biomarker for disease activity.
galectin-3 content allows evaluate myocardial dysfunction in asymptomatic patients with congenital heart defects after surgical correction
High platelet ROCK activity and galectin-3 levels are associated with increased risk in arteriovenous shunt dysfunction.
Increased galectin 3 expression is associated with adverse cardiovascular events and all-cause mortality in type 2 diabetes.
High galectin-3 and low HDL-C was associated with primary outcome, recurrent stroke, and vascular events within 1 year after ischemic stroke.
the protective role of Gal-3 inhibition in the kidney injury was shown to be mediated by protein kinase C alpha (PKC-a), which promoted cell apoptosis and collagen I synthesis in HEK293 cells. These results demonstrated the potential Gal-3 and PKC-alpha as therapeutic targets for the treatment of acute kidney injury (AKI) and chronic kidney diseases (CKD)
Local tissue invasion and destruction by hepatic venous malformation may be related to the upregulation of Gal-3.
Serum GAL3 was significantly elevated in patients with arrhythmogenic right ventricular cardiomyopathy. GAL3 levels were higher in patients with VT/VF as compared with those without VT/VF.
serum level increased significantly according to the different stages of impaired left atrial function
Data show that patients with atrial fibrillation (AF) had significantly higher galectin-3 plasma levels and high-sensitivity C-reactive protein (hs-CRP) oncentration compared with patients without AF.
Gal-3 serum level predicts the response to cardiac resynchronization therapy at 6 months and long-term outcomes in chronic heart failure patients.
Exosomes Derived from HIV-1 Infected DCs Mediate Viral trans-Infection via Fibronectin and Galectin-3.
Gal-1 and Gal-3 through their binding partners may form a supramolecular structure at the cell surface of fibroblasts, immune cells, endothelial cells, and in the extracellular space that might influence the fibroblast morphology, adhesion, proliferation, migration, and survival as well as the inflammatory responses.
Data found that pathological B-cells from patients with chronic lymphocytic leukemia (CLL) exhibit increased expression of Gal-3. Moreover, the study suggests that the highest expression of Gal-3 is associated with 17p deletion in CLL.
promotes cancer cell adhesion to vascular endothelial cells by increasing the expression of N-cadherin and CD44 via an increase of beta-catenin nuclear accumulation
Our results suggest a direct role for Gal-3 in Paracoccidioides brasiliensis infection, with beneficial effects for the mammalian host.
Increased circulating Gal3 is associated with increased 12 months cumulative cardiovascular events among patients with documented non-Hodgkin lymphoma.
Galectin-1 and galectin-3 are overexpressed in renal cell carcinoma with different percentage in different subtypes
hibition of Galectin-3 gene expression in oral squamous cell carcinoma can significantly reduce the proliferation and invasion of cancer cells and induce apoptosis. The mechanism is related to downregulation of the Wnt/beta-catenin signaling pathway.
Rs2274273 and rs17128183 rare allele bearing genotypes, according to the dominant model (CT+TT vs. CC and AG+GG vs. AA, respectively), were significantly and independently associated with maladaptive LVR (adjusted OR = 3.02, P = 0.016; adjusted OR = 3.14, P = 0.019, respectively) and higher LGALS-3 mRNA expression
Mutational tuning of galectin-3 specificity and biological function.
The overall findings suggest that the secreted galectin-3 stimulated by PGF plays a role in structural luteolysis by binding to beta 1 integrin.
The relative abundance of PIBF, LGALS1, LGALS3, LGALS3BP, and LGALS9 mRNA would display a differential expression pattern in the endometrium.
this study shows that galectin-3 deficiency enhances type 2 immune cell-mediated myocarditis in mice
Mice lacking galectin-3 (Lgals3) function have decreased home cage movement
endogenous galectin-3 enhances the effects of H5N1 infection by promoting host inflammatory responses and regulating IL-1beta production by macrophages via interaction with NLRP3.
Gal-3 contributes to the pathogenesis of ocular allergy and represents a relevant therapeutic target.
this study shows that decrease of galectin-3 in keratinocytes is a potential diagnostic marker and a critical contributor to the pathogenesis of psoriasis
Compared with WT mice, Gal-3 KO mice have more germinal centers B cells and T follicular helper cells, increased percentages of antibody-secreting cells and higher concentrations of immunoglobulins and IFN-gamma in serum, and develop a lupus-like disease.
Evidence for a contribution of galectin-3 to bone cell maturation and function, bone remodeling, and biomechanical competence, thus identifying galectin-3 as a promising therapeutic target for age-related disorders of bone remodeling.
Robust upregulation of cardiac galectin-3 (Gal-3) expression in a mouse model of cardiomyopathy attributable to cardiomyocyte-restricted transgenic activation of beta2-adrenoceptors may not be a critical disease mediator of cardiac remodeling in this model.
It has been reported that the Galectin-3/NuMA interaction is functionally important for the spindle pole organization; spindle pole cohesion requires glycosylation-mediated localization of NuMA.
Galectin-3 suppresses antibacterial autophagy through a host N-glycan-dependent mechanism in Listeria-infected macrophages. Knock out of the galectin-3 gene resulted in enhanced LC3 recruitment to Listeria and decreased bacterial replication.
Study shows that potent pro-inflammatory and pro-fibrotic molecules, osteopontin and galectin-3, are not major disease modulators of laminin alpha2 chain-deficient muscular dystrophy.
These results suggest that following head trauma, released galectin-3 may act as an alarmin, binding, among other proteins, to TLR-4 and promoting inflammation and neuronal loss.
Gal-3 and nSMase, by inducing thyroid changes, might be the cause of the increased expression and altered distribution of TSH, thyroglobulin, and TSHR or vice-versa.
Stroke (after left sided permanent middle cerebral artery occlusion) triggers central and peripheral galectin-3 release causing enteric neuronal loss through a TLR4 mediated mechanism involving TAK1 and AMPK.
the secretion of galectin-3 as a novel mechanism for osteoblasts to control osteoclastogenesis and to maintain trabecular bone homeostasis independently of the RANKL/OPG-axis.
Our findings establish gal-3 as a molecular regulator of the JAG1/Notch-1 signaling pathway and have direct implications for the development of strategies aimed at controlling tumor angiogenesis.
Mycobacerium PtkA downregulates host Galectin 3, which is an anti-apoptotic molecule.
Antilymphoma activity by M(IFN-gamma/LPS) macrophages was mediated, in part, by galectin-3. Intriguingly, aggressive lymphoma growth was markedly impaired in mice deficient in galectin-3, suggesting either that host galectin-3-mediated antilymphoma activity is required to sustain net tumor growth or that additional functions of galectin-3 drive key oncogenic mechanisms in non-Hodgkin's lymphoma.
This gene encodes a member of the galectin family of carbohydrate binding proteins. Members of this protein family have an affinity for beta-galactosides. The encoded protein is characterized by an N-terminal proline-rich tandem repeat domain and a single C-terminal carbohydrate recognition domain. This protein can self-associate through the N-terminal domain allowing it to bind to multivalent saccharide ligands. This protein localizes to the extracellular matrix, the cytoplasm and the nucleus. This protein plays a role in numerous cellular functions including apoptosis, innate immunity, cell adhesion and T-cell regulation. Alternate splicing results in multiple transcript variants.
35 kDa lectin
, beta-galactosides-binding lectin
, carbohydrate-binding protein 35
, galactose-specific lectin 3
, igE-binding protein
, laminin-binding protein
, lectin L-29
, lectin, galactoside-binding, soluble, 3 (galectin 3)
, mac-2 antigen
, 3 (galectin 3)
, CBP 35
, IgE-binding protein
, MAC-2 antigen
, lectin, galactoside-binding, soluble, 3
, galectin 3
, IgE binding protein
, lectin, galactose binding, soluble 3
, L-34 galactoside-binding lectin