Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.4.99.6 (sialyltransferase)
 1,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat serum was found to contain an inhibitor of pure alpha2-6 sialyltransferase (EC 2.4.99.1). The inhibitor was a high Mr protein isolated by molecular filtration on Sephadex G100, followed by anion exchange chromatography on Sephadex DEAE A25, then separation on Sepharose CL 4B, and finally by isoelectric focusing. Electrophoretic separation and subsequent N-terminal sequence analysis of the active inhibitor preparation showed the presence of two protein components, identified as rat C-reactive protein, and rat alpha1 macroglobulin. Pure rat CRP did not inhibit alpha2-6 sialyltransferase. Treatment of the inhibitor preparations with monospecific antibodies against rat alpha1 macroglobulin blocked inhibitory activity in a dose-dependent manner. The results present strong evidence that alpha1 macroglobulin is capable of acting as an inhibitor of alpha2-6 sialyltransferase. No inhibition of galactosyltransferase (EC 2.4.1.38) could be detected, indicating that the interaction with alpha1 macroglobulin may have specificity among the glycosyltransferases. The entrapment of alpha2-6 sialyltransferase by alpha1 macroglobulin presented here occurs in vitro and will require further in vivo investigations to determine the precise physiological significance. Independent of the physiologic significance is the finding that this interaction occurs in vitro, which, pending elucidation of the precise mechanism and specificity, may provide a new tool for investigations into the functional significance of sialylation, and potentially for use or design of new inhibitors of therapeutic value in physiologic conditions involving altered levels of sialylation.
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PMID:Identification of rat alpha1 macroglobulin as an inhibitor of rat Galbeta1-4GlcNAc alpha2-6 sialyltransferase. 937 81

Assessment of influenza virus disease progression and efficacy of antiviral therapy in the widely used mouse models relies mostly on body weight loss and lung virus titers as markers of disease. However, both parameters have their shortcomings. Therefore, the aim of our study was to find non-invasive markers in the murine model of severe influenza that could detect disease early and predict disease outcome. BALB/c mice were lethally infected with influenza A(H1N1)pdm09 virus and serum samples were collected at various time points. Enzyme-linked immunosorbent assays were performed to quantify amounts of serum amyloid A (SAA), C-reactive protein, complement 3, transferrin, corticosterone, prostaglandin E2, H2O2, and alpha-2,6-sialyltransferase. We found that SAA was the most promising candidate with levels acutely and temporarily elevated by several hundred-fold 3 days post virus inoculation. Upon treatment with oseltamivir phosphate, levels of SAA were significantly decreased. High levels of SAA were associated with poor disease prognosis, whereas body weight loss was not as a reliable predictor of disease outcome. SAA levels were also transiently increased in BALB/c mice infected with influenza A(H3N2) and influenza B virus, as well as in C57BL/2, Swiss-Webster, and DBA.2 mice infected with influenza A(H1N1)pdm09 virus. High levels of SAA often, but not always, were associated with disease outcome in these other influenza virus mouse models. Therefore, SAA represents a valid biomarker for influenza disease detection in all tested mouse strains but its prognostic value is limited to BALB/c mice infected with influenza A(H1N1)pdm09 virus.
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PMID:Serum amyloid A (SAA) is an early biomarker of influenza virus disease in BALB/c, C57BL/2, Swiss-Webster, and DBA.2 mice. 2752 92