Study identifies NRP2 and ESL-1 as targets for polysialylation in murine microglia and human THP-1 macrophages and reveals a striking convergence in the regulation of the two polysialylated acceptors in the course of inflammatory activation. A pool of polysialylated NRP2 and ESL-1 is assembled after injury or in culture and its shedding is an early response to lipopolysaccharide-induced activation of microglia. | Polysialylation and lipopolysaccharide-induced shedding of E-selectin ligand-1 and neuropilin-2 by microglia and THP-1 macrophages. Werneburg S, Buettner FF, Erben L, Mathews M, Neumann H, Mühlenhoff M, Hildebrandt H. | 01/6/2018 |
Our results highlight the fact that interaction between APN and ESL-1 could provide a fundamental mechanism underlying the anti-atherogenic properties of APN. | E-selectin ligand-1 (ESL-1) is a novel adiponectin binding protein on cell adhesion. Yamamoto H, Kuroda N, Uekita H, Kochi I, Matsumoto A, Niinaga R, Funahashi T, Shimomura I, Kihara S. | 06/28/2016 |
circulating prostate cancer cells' rolling capacity contributes to metastasis, and that is in part controlled by ESL-1. | E-selectin ligand-1 controls circulating prostate cancer cell rolling/adhesion and metastasis. Yasmin-Karim S, King MR, Messing EM, Lee YF., Free PMC Article | 10/3/2015 |
Studies indicate that PSGL-1, CD44, and ESL-1 on mature leukocytes are physiologic glycoprotein ligands for endothelial P-selectin and E-selectin. | Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow. Zarbock A, Ley K, McEver RP, Hidalgo A., Free PMC Article | 03/24/2012 |
expression of Cfr in the Golgi apparatus and on the plasma membrane is finely tuned through two distinct mechanisms for exhibiting different functions. | Retention in the Golgi apparatus and expression on the cell surface of Cfr/Esl-1/Glg-1/MG-160 are regulated by two distinct mechanisms. Miyaoka Y, Kato H, Ebato K, Saito S, Miyata N, Imamura T, Miyajima A. | 12/24/2011 |
C2GnT1 gene expression and the resulting C2-O-sLe(X) carbohydrates produced mediate the adhesive and invasive behaviors of human carcinomas which may influence their metastatic potential. | C2-O-sLeX glycoproteins are E-selectin ligands that regulate invasion of human colon and hepatic carcinoma cells. St Hill CA, Baharo-Hassan D, Farooqui M., Free PMC Article | 08/6/2011 |
Observational study of gene-disease association. (HuGE Navigator) | Fine mapping and association studies of a high-density lipoprotein cholesterol linkage region on chromosome 16 in French-Canadian subjects. Dastani Z, Pajukanta P, Marcil M, Rudzicz N, Ruel I, Bailey SD, Lee JC, Lemire M, Faith J, Platko J, Rioux J, Hudson TJ, Gaudet D, Engert JC, Genest J., Free PMC Article | 12/2/2009 |
Genome-wide association study of gene-disease association. (HuGE Navigator) | A pilot genome-wide association study of early-onset breast cancer. Kibriya MG, Jasmine F, Argos M, Andrulis IL, John EM, Chang-Claude J, Ahsan H. | 12/2/2009 |
under hypoxia, ESL-1 is shed from activated hepatic stellate cells | Expression of E-selectin ligand-1 (CFR/ESL-1) on hepatic stellate cells: implications for leukocyte extravasation and liver metastasis. Antoine M, Tag CG, Gressner AM, Hellerbrand C, Kiefer P. | 01/21/2010 |
evaluated in human brain tumors exhibiting varying degrees of malignancy | Identification of MG-160, a FGF binding medial Golgi sialoglycoprotein, in brain tumors: an index of malignancy in astrocytomas. Yamaguchi F, Morrison RS, Gonatas NK, Takahashi H, Sugisaki Y, Teramoto A. | 01/21/2010 |
a novel variant of the GLG1 gene product called GLG2 is reported; genetic analysis suggests GLG1 & GLG2 are the products of a single gene, the mRNA of which can be processed by alternative splicing to generate different transcripts encoding GLG1 or GLG2 | A novel isoform of human Golgi complex-localized glycoprotein-1 (also known as E-selectin ligand-1, MG-160 and cysteine-rich fibroblast growth factor receptor) targets differential subcellular localization. Ahn J, Febbraio M, Silverstein RL. | 01/21/2010 |