{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nasirikenari M"],"funding":["NIAID NIH HHS","Roswell Park Cancer Institute's National Cancer Institute-funded Cancer Center","NCI NIH HHS","NIH"],"pagination":["457-66"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2830128"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["87(3)"],"pubmed_abstract":["Cumulative evidence indicates that the sialyltransferase ST6Gal-1 and the sialyl-glycans, which it constructs, are functionally pleiotropic. Expression of the ST6Gal-1 gene is mediated by six distinct promoter/regulatory regions, and we hypothesized that these promoters may be used differentially to produce ST6Gal-1 for different biologic purposes. To examine this hypothesis, we compared a mouse with a complete deficiency in ST6Gal-1 (Siat1 null) with another mouse that we have created previously with a disruption only in the P1 promoter (Siat1DeltaP1). We noted previously greater neutrophilic inflammation associated with ST6Gal-1 deficiency. Here, we report that ST6Gal-1-deficient mice also have significantly elevated eosinophilic responses. Upon i.p. thioglycollate elicitation, eosinophi"],"journal":["Journal of leukocyte biology"],"pubmed_title":["Altered eosinophil profile in mice with ST6Gal-1 deficiency: an additional role for ST6Gal-1 generated by the P1 promoter in regulating allergic inflammation."],"pmcid":["PMC2830128"],"funding_grant_id":["AI056082","P30 CA016056","CA16056","R21 AI078429","R01 AI056082","AI078429"],"pubmed_authors":["Segal BH","Lau JT","Thanavala Y","Chandrasekaran EV","Lee JJ","Nasirikenari M","Matta KL","Bogner PN","Lugade AA"],"additional_accession":[]},"is_claimable":false,"name":"Altered eosinophil profile in mice with ST6Gal-1 deficiency: an additional role for ST6Gal-1 generated by the P1 promoter in regulating allergic inflammation.","description":"Cumulative evidence indicates that the sialyltransferase ST6Gal-1 and the sialyl-glycans, which it constructs, are functionally pleiotropic. Expression of the ST6Gal-1 gene is mediated by six distinct promoter/regulatory regions, and we hypothesized that these promoters may be used differentially to produce ST6Gal-1 for different biologic purposes. To examine this hypothesis, we compared a mouse with a complete deficiency in ST6Gal-1 (Siat1 null) with another mouse that we have created previously with a disruption only in the P1 promoter (Siat1DeltaP1). We noted previously greater neutrophilic inflammation associated with ST6Gal-1 deficiency. Here, we report that ST6Gal-1-deficient mice also have significantly elevated eosinophilic responses. Upon i.p. thioglycollate elicitation, eosinophi","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Mar","modification":"2025-04-21T14:29:24.697Z","creation":"2019-03-27T00:28:57Z"},"accession":"S-EPMC2830128","cross_references":{"pubmed":["20007243"],"doi":["10.1189/jlb.1108704"]}}