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Ajit Varki

Researcher at University of California, San Diego

Publications -  557
Citations -  63836

Ajit Varki is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Sialic acid & SIGLEC. The author has an hindex of 124, co-authored 542 publications receiving 58772 citations. Previous affiliations of Ajit Varki include Emory University & National Institute of Advanced Industrial Science and Technology.

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Journal ArticleDOI

Coevolution of Siglec-11 and Siglec-16 via gene conversion in primates.

TL;DR: It is indicated that Siglec-11 and SigleC-16 have been maintained as paired receptors by repeated gene conversions under relaxed functional constraints in the primate lineage.
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An IgG Monoclonal Antibody against Dictyostelium discoideum Glycoproteins Specifically Recognizes Fucα1,6GlcNAcβ in the Core of N-Linked Glycans LOCALIZED EXPRESSION OF CORE-FUCOSYLATED GLYCOCONJUGATES IN HUMAN TISSUES

TL;DR: These antibodies show that many proteins in human tissues are core-fucosylated, but their expression is localized to skin keratinocytes, vascular and visceral smooth muscle cells, epithelia, and some extracellular matrix-like material surrounding subpopulations of lymphocytes.
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Studies on the Detection, Expression, Glycosylation, Dimerization, and Ligand Binding Properties of Mouse Siglec-E

TL;DR: Sialoglycan array studies indicate that this modification has complex effects on recognition by Siglec-E, in relationship to the underlying structures, but there are no differences in phosphorylation or SHP-1 recruitment between dimeric and monomeric SigleC-E expressed on HEK293A cells.
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Enhanced T cell function in a mouse model of human glycosylation.

TL;DR: It is reported that Cmah−/− mice T cells proliferate faster and have greater expression of activation markers than wild-type mouse T cells, and a uniquely human glycosylation mutation, modeled in mice, leads to a more proliferative and active T cell population.
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Tamm–Horsfall glycoprotein engages human Siglec-9 to modulate neutrophil activation in the urinary tract

TL;DR: It is found that THP binds neutrophils and that this interaction reduces reactive oxygen species generation, chemotaxis and killing of UPEC, and data support THP as an important negative regulator of neutrophil activation in the urinary tract, with dual functions to counteract bacterial colonization and suppress excessive inflammation within the urine tract.