Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CD14 is a glycosylphosphatidyl-inositol (GPI)-linked, 55 kDa protein that binds bacterial lipopolysaccharide (LPS, endotoxin) and plays a key role in mediating cellular responses to this potent inflammatory stimulus. Binding of LPS to CD14 is facilitated by serum proteins such as LPS binding protein (LBP). To determine if there are additional plasma proteins that bind to CD14, plasma was passed over immobilized CD14 in the presence or absence of LPS, and retained proteins were eluted. This procedure isolated not only LBP but also a serum protein known as Mac-2-binding protein (Mac-2-BP), a 97 kDa species without a known function. Binding of both LBP and Mac-2-BP to CD14 required the simultaneous presence of LPS. Experiments with purified Mac-2-BP showed that this protein alone neither enabled responses of CD14-bearing cells to LPS nor blocked the ability of plasma to enable responses of CD14-bearing cells to LPS. However, Mac-2-BP did slow the neutralization of LPS mediated by plasma lipoprotein. These studies describe the first potential function for Mac-2-BP, and suggest that neutralization of LPS in plasma may be controlled by proteins in addition to LBP and CD14.
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PMID:LPS-dependent interaction of Mac-2-binding protein with immobilized CD14. 758 57

Many studies have implicated cell-surface lectins in heterologous cell-cell adhesion, but little is known about the participation of lectins in cellular adhesion in homologous cells. Here, we show the development of a cell model for investigating the direct role of a cell-surface lectin in homologous cell-cell adhesion. Parenchymal cells were isolated from caprine liver using a perfusion buffer, and dispersed in a chemically defined modified Ringer's solution. These cells undergo autoagglutination in the presence of Ca(2+). The autoagglutinated cells can be dissociated specifically with D-galactose (50 mM), which also inhibits the liver cell autoagglutination event. The blood serum protein fetuin has no effect on liver cell autoagglutination, whereas desialylated fetuin (100 microM), with its terminal D-galactose residue, showed a high affinity for blocking the autoagglutination event. The data demonstrates the occurrence of a Ca(2+)-dependent D-galactose-specific lectin and a lectin receptor on the parenchymal cells. Furthermore, it shows that the observed autoagglutination event is caused by the interaction of the cell-surface lectin with its receptor on the neighbouring homologous cells. The data supports the view that homologous cell-cell contact in mammalian tissues is triggered by such lectin-receptor interaction and that the previously reported cell-surface adhesive proteins serve as a secondary force to strengthen cell adhesion. This cell model could be extremely useful for investigating the direct role of cell-surface lectin and its receptor in homologous cell adhesion in a variety of tissues under normal and pathological conditions.
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PMID:Homologous liver parenchymal cell-cell adhesion mediated by an endogenous lectin and its receptor. 2033 7

Non-convulsive status epilepticus (NCSE) is a prolonged epileptic seizure with subtle symptoms that may delay clinical diagnosis. Emerging experimental evidence shows brain pathology and epilepsy development following NCSE. New diagnostic/prognostic tools are therefore needed for earlier and better stratification of treatment. Here we examined whether NCSE initiates a peripheral immune response in blood serum from rats that experienced electrically-induced NCSE. ELISA analysis showed an acute transient increase in serum protein levels including interleukin-6 6 h post-NCSE, similar to the immune reaction in the brain. At 4 weeks post-NCSE, when 75% of rats subjected to NCSE had also developed spontaneous seizures, several immune proteins were altered. In particular, markers associated with microglia, macrophages and antigen presenting cells, such as CD68, MHCII, and galectin-3, were increased and the T-cell marker CD4 was decreased in serum compared to both non-stimulated controls and NCSE rats without spontaneous seizures, without correlation to interictal epileptiform activity. Analyses of serum following intracerebral injection of lipopolysaccharide (LPS) showed an acute increase in interleukin-6, but at 4 weeks unaltered levels of MHCII and galectin-3, an increase in CD8 and CD11b and a decrease in CD68. None of the increased serum protein levels after NCSE or LPS could be confirmed in spleen tissue. Our data identifies the possibility to detect peripheral changes in serum protein levels following NCSE, which may be related to the development of subsequent spontaneous seizures.
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PMID:Immune Profile in Blood Following Non-convulsive Epileptic Seizures in Rats. 3133 61