A
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.
Papers
More filters
Journal ArticleDOI
Advances in the Biology and Chemistry of Sialic Acids
Xi Chen,Ajit Varki +1 more
TL;DR: A large library of sialoside standards and derivatives in amounts sufficient for structure-activity relationship studies are provided and sialoglycan microarrays provide an efficient platform for quick identification of preferred ligands for sialic acid-binding proteins.
Journal ArticleDOI
P-selectin deficiency attenuates tumor growth and metastasis.
TL;DR: It is shown that P-selectin, which normally binds leukocyte ligands, can promote tumor growth and facilitate the metastatic seeding of a mucin-producing carcinoma.
Journal ArticleDOI
Synergistic effects of L- and P-selectin in facilitating tumor metastasis can involve non-mucin ligands and implicate leukocytes as enhancers of metastasis
TL;DR: L-selectin on neutrophils, monocytes, and/or NK cells has a role in facilitating metastasis, acting beyond the early time points wherein P- selectin mediates interactions of platelet with tumor cells.
Journal ArticleDOI
Differential interactions of heparin and heparan sulfate glycosaminoglycans with the selectins. Implications for the use of unfractionated and low molecular weight heparins as therapeutic agents.
TL;DR: High-dose unfractionated heparin should be investigated as a treatment option for acute and chronic diseases in which P- and L-selectin play pathological roles, and the current switchover to low-molecular weight heparins may come at some loss of this effect.
Journal ArticleDOI
Molecular mimicry of host sialylated glycans allows a bacterial pathogen to engage neutrophil Siglec-9 and dampen the innate immune response
TL;DR: GBS can impair neutrophil defense functions by coopting a host inhibitory receptor via sialoglycan molecular mimicry, a novel mechanism of bacterial immune evasion.