Galectin

About: Galectin is a research topic. Over the lifetime, 2076 publications have been published within this topic receiving 103409 citations. The topic is also known as: IPR001079 & Galectin.

Antisense galectin-3 alters thymidine incorporation in human MDA-MB435 breast cancer cells

Abstract: Galectin-3 is a 30-kDa galactose-binding protein member of the galectin family. Galectin-3 is involved in multiple intracellular and extracellular biological functions, e.g. interactions with laminin and with nucleic acids. This latter property is consistent with the presence of 3. serum-response factor-like domain at the amino-terminal part of the protein. Galectin-3 expression is upregulated during serum-mediated induction of proliferation. In order to examine the role of galectin-3 in breast cancer cell proliferation, we examined in this study the influence of antisense galectin-3 complementary DNA stable transfection on the in vitro thymidine incorporation of human breast cancer MDA-MB435 cells. Two stable transfectants, clones 5.24 and 5.29, were selected based both on the presence of a complete CMV promoter-antisense galectin-3 cDNA cassette as assayed by polymerase chain reaction, and on efficient down-regulation of galectin-3 protein expression as determined by Western blotting. Thymidine incorporation experiments showed that both clones were characterized by significantly decreased values of DNA incorporation compared to wild-type transfectants (55 to 68%, and 71 to 82% of the control clone values). Our data demonstrate for the first time that galectin-3 decreases thymidine incorporation in breast cancer cells. The mechanism underlying this property of galectin-3 and its importance during breast cancer development remain to be elucidated.

Characterization of galectin-1 from Chinese giant salamanders Andrias davidianus and its involvements during immune response.

Abstract: Galectins are considered as a multifunctional protein which play essential roles in cell adhesion and apoptosis, inflammation, tumor progression and immune response. In spite of extensive studies of galectin importance in immune system among different animals, few studies have been devoted to their functions in amphibian. In the present study, we characterized one proto type of galectin (named AdGal1) from Chinese giant salamander Andrias davidianus and studied its function in immune response. AdGal1 cDNA possesses an open reading frame of 598 bp, which encodes a putative galectin of 134 amino acids containing one carbohydrate recognition domains (CRDs). The constitutive expression of mRNA transcripts was detected in a wide range of tissues, with the highest expression in kidney. Immune challenges with Aeromonas hydrophila and Chinese giant salamander iridovirus (GSIV), the transcript level of AdGal1 in kidney was significantly upregulated. The mature protein of AdGal1 was successfully expressed and purified in Escherichia coli BL21 (DE3). The recombinant AdGal1 (rAdGal1) could show bind activity to different Gram negative and Gram positive bacteria. It could also strongly agglutinate different kinds of bacteria at different concentrations. Collectively, these data from the present study indicate that AdGal1 is a vital pattern recognition receptor to recognize different microbes in the innate immune system of Andrias davidianus.

Full-length galectin-8 and separate carbohydrate recognition domains: the whole is greater than the sum of its parts?

Abstract: Galectin-8 (Gal-8) is a tandem-repeat type galectin with affinity for β-galactosides, bearing two carbohydrate recognition domains (CRD) connected by a linker peptide The N- and C-terminal domains (Gal-8N and Gal-8C) share 35% homology, and their glycan ligand specificity is notably dissimilar: while Gal-8N shows strong affinity for α(2-3)-sialylated oligosaccharides, Gal-8C has higher affinity for non-sialylated oligosaccharides, including poly-N-acetyllactosamine and/ or A and B blood group structures Particularly relevant for understanding the biological role of this lectin, full-length Gal-8 can bind cell surface glycoconjugates with broader affinity than the isolated Gal-8N and Gal-8C domains, a trait also described for other tandem-repeat galectins Herein, we aim to discuss the potential use of separate CRDs in modelling tandem-repeat galectin-8 and its biological functions For this purpose, we will cover several aspects of the structure-function relationship of this protein including crystallographic structures, glycan specificity, cell function and biological roles, with the ultimate goal of understanding the potential role of each CRD in predicting full-length Gal-8 involvement in relevant biological processes

Under-Evaluated or Unassessed Pathogenic Pathways in Autoimmune Hepatitis and Implications for Future Management.

Abstract: Autoimmune hepatitis is a consequence of perturbations in homeostatic mechanisms that maintain self-tolerance but are incompletely understood. The goals of this review are to describe key pathogenic pathways that have been under-evaluated or unassessed in autoimmune hepatitis, describe insights that may shape future therapies, and encourage investigational efforts. The T cell immunoglobulin mucin proteins constitute a family that modulates immune tolerance by limiting the survival of immune effector cells, clearing apoptotic bodies, and expanding the population of granulocytic myeloid-derived suppressor cells. Galectins influence immune cell migration, activation, proliferation, and survival, and T cell exhaustion can be induced and exploited as a possible management strategy. The programmed cell death-1 protein and its ligands comprise an antigen-independent inhibitory axis that can limit the performance of activated T cells by altering their metabolism, and epigenetic changes can silence pro-inflammatory genes or de-repress anti-inflammatory genes that affect disease severity. Changes in the intestinal microbiota and permeability of the intestinal mucosal barrier can be causative or consequential events that affect the occurrence and phenotype of immune-mediated disease, and they may help explain the female propensity for autoimmune hepatitis. Perturbations within these homeostatic mechanisms have been implicated in experimental models and limited clinical experiences, and they have been favorably manipulated by monoclonal antibodies, recombinant molecules, pharmacological agents or dietary supplements. In conclusion, pathogenic mechanisms that have been implicated in other systemic immune-mediated and liver diseases but under-evaluated or unassessed in autoimmune hepatitis warrant consideration and rigorous evaluation.