A cloned CD15s‐negative variant of HL60 cells is deficient in expression of FUT7 and does not adhere to cytokine‐stimulated endothelial cells

Weston, Brent W.; Hiller, Kara M.; Mayben, John P.; Manousos, George A.; Nelson, Christine E.; Klein, Marina B.; Goodman, Jesse L.

doi:10.1111/j.1600-0609.1999.tb01849.x

Cited by 11 publications

(4 citation statements)

References 25 publications

(19 reference statements)

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“…Treatment of human HL-60 cells for 3 days led to almost complete abolition of Lewis X (Le X , Galβ1,4[α1,3Fuc]GlcNAcβOR) and Sialyl Lewis X (SLe x , NeuAcα2,3Galβ1,4[α1,3Fuc]GlcNAcβOR), as assessed by flow cytometry with labeled antibodies specific for these two epitopes ( Figure 2a-b ), which in this cell line are products of the FUT4 and FUT7 enzymes, respectively 26,27 . Treatment of CHO cells, commonly used to produce bio-therapeutic proteins, resulted in dramatic reduction of core fucosylation of N-linked glycans, a product of FUT8, as probed by the AAL lectin ( Figure 2c ).…”

Section: Resultsmentioning

confidence: 91%

Global metabolic inhibitors of sialyl- and fucosyltransferases remodel the glycome

et al. 2012

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Despite the fundamental roles of sialyl- and fucosyltransferases in mammalian physiology, there are few pharmacological tools to manipulate their function in a cellular setting. Although fluorinated analogs of the donor substrates are well-established transition state inhibitors of these enzymes, they are not membrane permeable. By exploiting promiscuous monosaccharide salvage pathways, we show that fluorinated analogs of sialic acid and fucose can be taken up and metabolized to the desired donor substrate-based inhibitors inside the cell. Due to the existence of metabolic feedback loops, they also act to prevent the de novo synthesis of the natural substrates, resulting in a global, family-wide shutdown of sialyl- and/or fucosyltransferases and remodeling of cell surface glycans. As an example of the functional consequences, the inhibitors drastically reduce expression of the sialylated and fucosylated ligand Sialyl Lewis X on myeloid cells, resulting in loss of binding to selectins and impaired leukocyte rolling.

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Section: Resultsmentioning

confidence: 91%

Global metabolic inhibitors of sialyl- and fucosyltransferases remodel the glycome

et al. 2012

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“…sLe a is elevated in a variety of carcinomas, particularly those of the pancreas, stomach, and colon. Detection of sLe a in pre-and postoperative serum is predictive of increased cancer mortality [37]. The association of high levels of serum sLe a with tumor invasion is common in patients with cancer [6,17,23,24].…”

Section: Biosynthesis Expression and Roles Of The Abh Lewis And Smentioning

confidence: 99%

Human Blood Group ABH/Ii, Lea,b,x,y, and Sialyl Lea,x Glycotopes; Internal Structures; and Immunochemical Roles of Human Ovarian Cyst Glycoproteins

2011

Advances in Experimental Medicine and Biology

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“…The functional α-(1,3) fucosyltransferases for LeX synthesis include Fut4 [4] and Fut9 [5]. Fut7 can only synthesize sialylated LeX [6], while the catalytic activity of Fut11 , a novel α-(1,3) fucosyltransferase, is only verified in human, so far [7]. …”

Section: Introductionmentioning

confidence: 99%

Different Effects of Androgen on the Expression of Fut1, Fut2, Fut4 and Fut9 in Male Mouse Reproductive Tract

Wang

et al. 2013

IJMS

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The α-(1,2) fucosyltransferases (Fut1 and Fut2) and α-(1,3) fucosyltransferases (Fut4, Fut9) are responsible for the synthesis of Lewis X (LeX) and Lewis Y (LeY) conjugated to glycoproteins. We recently reported that these fucosyltransferases were differentially expressed in the reproductive tract of male mouse. Here, we studied the effect of androgen on fucosyltransferase expression through the use of mouse castration models. We found that Fut1 mRNA and Fut4 mRNA were upregulated, while Fut2 mRNA and Fut9 mRNA were downregulated by androgen in the caput epididymis. However, in the vas deferens and prostate, only Fut4 mRNA and Fut2 mRNA were respectively upregulated following exposure to androgen. In the seminal vesicle, all fucosyltransferases, with the exception of Fut9, were upregulated. We identified the androgen receptor binding sites (ARBSs) of Fut2, Fut4 and Fut9 in the caput epididymis. Luciferase assay for these ARBSs is able to provide an indication as to why Fut4 and Fut9 are differently expressed and regulated by androgen, although they catalyze the same α-(1,3) fucose linkage. Our study showed that androgen could differentially regulate the expression of these fucosyltransferases and provided an insight into the characteristic distribution of each fucosyltransferase responsible for LeX/LeY biosynthesis in the male reproductive tract.

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A cloned CD15s‐negative variant of HL60 cells is deficient in expression of FUT7 and does not adhere to cytokine‐stimulated endothelial cells

Cited by 11 publications

References 25 publications

Global metabolic inhibitors of sialyl- and fucosyltransferases remodel the glycome

Global metabolic inhibitors of sialyl- and fucosyltransferases remodel the glycome

Human Blood Group ABH/Ii, Lea,b,x,y, and Sialyl Lea,x Glycotopes; Internal Structures; and Immunochemical Roles of Human Ovarian Cyst Glycoproteins

Different Effects of Androgen on the Expression of Fut1, Fut2, Fut4 and Fut9 in Male Mouse Reproductive Tract

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