Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have characterized a glycosphingolipid (GSL) receptor for Staphylococcus enterotoxin-B (SEB) in cultured human kidney proximal tubular (PT) cells. Solid-phase binding of [125I]SEB to the GSL receptor was concentration dependent and was not displaceable by two structurally related toxins, such as staphylococcal enterotoxin-A and toxic shock syndrome toxin-1. Rat kidney cells did not bind [125I]SEB. However, when the rat kidney cells were pre-incubated with digalactosylceramide, there was a concentration-dependent binding of [125I]SEB. Trimethylsilyl derivatization of methyl glycosides, followed by gas-liquid chromatography-mass spectrometry (GC-MS), revealed that galactose was the major sugar component of this putative receptor GSL. The sphingosines present in this GSL were d18:2, d22:2 and d23:0; the fatty acids present were palmitate, oleate and stearate. Permethylation of alditol acetates and GC-MS revealed two predominant sugars, namely 2, 3, 4 and 6 tetramethylgalactital and 2, 3 and 6 trimethylgalactital. The GSL receptor for SEB was sensitive to alpha-galactosidase, and resistant to beta-galactosidase and beta-glucosidase. Taken together, our studies reveal that the tentative structure of the receptor for SEB in human kidney PT cells is CerGal alpha 1-->4Gal. In summary, we have identified a GSL as one of the binding sites of SEB, a food-borne toxin. We believe that our finding may open up rational approaches for the therapy of SEB-induced glycopathology in man.
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PMID:Digalactosylceramide is the receptor for staphylococcal enterotoxin-B in human kidney proximal tubular cells. 765 70

A continuous culture technique utilising a variant of Staphylococcus aureus 8325-4 containing transcriptional gene fusions was used to investigate the relationships between cell density (OD(600)), steady-state specific growth rate (mu) and expression of both agr (accessory gene regulator) and tst (toxic shock syndrome toxin-1). The expression of these genes was assessed by two single-copy independently arranged chromosomal-based reporter systems, beta-galactosidase agr-P3 promoter fusion and a lux-tst promoter fusion. Cell density and specific agr expression were found to be positively correlated. In the model, the minimum cell density predicted to promote specific agr expression was an OD(600) of 0.14, equivalent to 1.2x10(8) CFU ml(-1). No direct relationship between cell density and specific tst expression was detected. Specific expressions of agr and tst were not correlated with specific growth rate and there appeared to be no direct link between agr and tst specific expression. The results support the hypothesis that agr is a functional unit of quorum sensing and that the amount of specific expression of tst is modulated independently of agr.
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PMID:The effect of cell density and specific growth rate on accessory gene regulator and toxic shock syndrome toxin-1 gene expression in Staphylococcus aureus. 1258 20