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1 beta-galactoside alpha2,6-sialyltransferase (ST6Gal-I).
2 beta-galactoside:alpha2-6-sialyltransferase (ST6Gal-I).
3 -galactosamide alpha-2,6-sialyltranferase I (ST6Gal-I).
4 tial for proper conformation and activity of ST6Gal I.
5 role of the S-sialylmotif of the same enzyme ST6Gal I.
6 lects for clonal variants with more abundant ST6Gal-I.
7 lylation of these integrins with recombinant ST6Gal-I.
8 olon epithelial cell line lacking endogenous ST6Gal-I.
9 and GnT-II or trans-Golgi enzymes GalT-I and ST6Gal-I.
10 and not on alpha2,6-sialic acids produced by ST6Gal-I.
11 ding is attenuated upon forced expression of ST6Gal-I.
12 ynthesized 13C-CMP-NeuAc to the desialylated ST6Gal-I.
13                                              ST6Gal I, a glycosyltransferase expressed by B cells, ca
14 at the coordinate up-regulation of gal-3 and ST6Gal-I, a feature that is characteristic of colon carc
15                             Correspondingly, ST6Gal-I activity augments the expression of tumor-promo
16                 Intriguingly, differences in ST6Gal-I activity do not affect the function of DR4 or D
17 heroid growth, and clonal variants with high ST6Gal-I activity preferentially survived in CSC culture
18 ated DNA damage, indicating that suppressing ST6Gal-I activity sensitizes inherently resistant cells
19 view summarizes the evidence suggesting that ST6Gal-I activity serves as an "off switch" for galectin
20 g TNFR1 at the cell surface via sialylation, ST6Gal-I acts as a functional switch to divert signaling
21                                              ST6Gal-I adds an alpha2,6-linked sialic acid to the term
22                     The glycosyltransferase, ST6Gal-I, adds sialic acid in an alpha2-6 linkage to the
23                                              ST6Gal-I (alpha2,6-sialyltransferase) is expressed as tw
24                   Sialylation of CD45 by the ST6Gal I also prevented galectin-1-induced clustering of
25                                              ST6Gal-I also augmented tumor-initiating potential.
26                                              ST6Gal-I also potentiates expression of the cell cycle r
27                                              ST6Gal-I also promoted resistance to gemcitabine and ena
28  precursor protein and the sialyltransferase ST6Gal I and is important in the pathogenesis of Alzheim
29 an nodes provided novel evidence for altered ST6Gal-I and GnT-IV glycotransferase activities in lung
30 cans and by other sialyltransferases such as ST6Gal-I and ST6GalNAc-I, forming alpha2,6-sialylated co
31 y 50% of colon adenocarcinomas) up-regulates ST6Gal-I and, in turn, increases sialylation of beta1 in
32 e in the expression of the sialyltransferase ST6Gal I, and an increase in the expression of the galac
33 lation, we forced constitutive expression of ST6Gal-I, and found that this strongly inhibited PMA-ind
34               Together, these findings place ST6Gal-I as a critical player in imparting gemcitabine r
35           These findings indicate a role for ST6Gal-I as a mediator of tumor progression, with its ex
36                 Recipient mice that received ST6Gal I(-/-) B cells demonstrated reduced influenza-spe
37  that in many ways carries an imprint of the ST6Gal-I binding site.
38 rum deprivation, supporting the concept that ST6Gal-I confers a survival advantage.
39 yposialylation), through BACE1 inhibition or ST6Gal-I constitutive overexpression, eliminates VCAM-1
40 ialic acid residues were also observed, with ST6Gal-I deficiency causing loss on endothelium and ST3G
41           Diminished immune responses due to ST6Gal-I deficiency further correlate with constitutive
42 date the mechanisms involved, we report that ST6Gal-I deficiency induces immunoglobulin M (IgM) antig
43 ed the subcellular location and mechanism of ST6Gal I dimer formation, as well as the role of Cys res
44 ed increased dimer formation suggesting that ST6Gal I dimers may be critical in the oligomerization p
45                       U937 cells with forced ST6Gal-I displayed TNFR1 with elevated alpha2-6 sialylat
46   Pulse-chase analysis demonstrated that the ST6Gal I disulfide-bonded dimer forms in the endoplasmic
47                                   Preventing ST6Gal-I down-regulation (and therefore integrin hyposia
48                                 Importantly, ST6Gal-I down-regulation results from cleavage by the BA
49 EK, but not phosphoinositide 3-kinase, block ST6Gal-I down-regulation, integrin hyposialylation, and
50 estingly, macrophage differentiation induces ST6Gal-I down-regulation, leading to reduced alpha2-6 si
51  inhibits galectin-1 death, we expressed the ST6Gal I enzyme in a galectin-1-sensitive murine T cell
52      SAalpha2,6Gal sequences, created by the ST6Gal I enzyme, are present on medullary thymocytes res
53 e for the first time the in vivo role of the ST6Gal-I enzyme in the growth and differentiation of spo
54 spondingly, at these later time points, high ST6Gal-I expressers displayed sustained activation of th
55 atient-derived xenograft tumors enriched for ST6Gal-I-expressing cells relative to pair-matched untre
56                                              ST6Gal I expression abrogated the reduction in CD45 tyro
57                                              ST6Gal I expression reduced galectin-1 binding to the ce
58  cells following viral infection, suggesting ST6Gal I expression remains high on activated B cells in
59              We demonstrate that the loss of ST6Gal I expression results in similar influenza infecti
60                                   Modulating ST6Gal-I expression in pancreatic and ovarian cancer cel
61 tive enrichment in clonal variants with high ST6Gal-I expression is observed upon prolonged serum dep
62 these results, serum-starved cells with high ST6Gal-I expression maintain a greater number of S phase
63                                   Similarly, ST6Gal-I expression was restricted to basal epidermal la
64                                  Blockade of ST6Gal-I expression with short interfering RNA reversed
65  PDAC cells, we found that knockdown (KD) of ST6Gal-I expression, as well as removal of surface alpha
66 tive enrichment of clonal variants with high ST6Gal-I expression, further substantiating a role for S
67 ls exhibited a corresponding upregulation of ST6Gal-I expression.
68                                              ST6Gal-I expressors (with alpha2-6 sialylated beta1 inte
69        Removal of alpha2-6 sialic acids from ST6Gal-I expressors by neuraminidase treatment restores
70   Finally, we show that beta1 integrins from ST6Gal-I expressors have increased association with tali
71 tal SW48 colonocytes (unsialylated), whereas ST6Gal-I expressors were protected.
72 er number of S phase cells compared with low ST6Gal-I expressors, reflecting enhanced proliferation.
73                 However, mechanisms by which ST6Gal-I facilitates tumor progression remain poorly und
74 Galbeta1-4GlcNAc:alpha2-6-sialyltransferase (ST6Gal I); formerly ST6N).
75 sferase of protein Asn-linked glycosylation (ST6Gal I) forms disulfide-bonded dimers that exhibit dec
76 HO-K1 cells indicated that expression of the ST6Gal I gene causes selective 9-O-acetylation of alpha2
77                           Thus, manipulating ST6Gal I gene expression may have therapeutic potential
78 D22 and ST6Gal-I knockout mice revealed that ST6Gal-I-generated B cell CD22L plays a role in splenic
79 c and BM-derived DCs, which does not contain ST6Gal-I-generated sialic acids and which, unlike the B
80 e oligomerization process involved in stable ST6Gal I Golgi localization.
81 sm is not the predominant mechanism used for ST6Gal I Golgi localization.
82     Although the recombinant soluble form of ST6Gal I has six cysteines, quantitative analysis indica
83 enon is reproducible by stable expression of ST6Gal I in parental CHO cells, but not upon transfectio
84 beta1-integrin function, we stably expressed ST6Gal-I in a colon epithelial cell line lacking endogen
85 xpression, further substantiating a role for ST6Gal-I in cell survival.
86  hairpin RNA (shRNA)-mediated attenuation of ST6Gal-I in colon carcinoma cells with elevated endogeno
87 hese results implicate a functional role for ST6Gal-I in fostering tumor cell survival within the ser
88    This first in vivo evidence for a role of ST6Gal-I in tumor progression was confirmed using a nove
89 ubset development, whereas the DC-associated ST6Gal-I-independent CD22L may be required for the maint
90 sfection of CHO-GD3-OAc(-) mutant cells with ST6Gal-I induced 9-O-acetylation specifically on sialyla
91                       Finally, we found that ST6Gal-I induced expression of the key tumor-promoting t
92                                          The ST6Gal I is a sialyltransferase that functions in the la
93                                          The ST6Gal I is expressed as two isoforms with a single amin
94 c cells and primary human CD14(+) monocytes, ST6Gal-I is down-regulated, leading to beta1 hyposialyla
95                                              ST6Gal-I is itself a glycoprotein, and in this initial a
96                            Here we show that ST6Gal-I is upregulated in ovarian and pancreatic carcin
97             The alpha-2,6-sialyltransferase (ST6Gal-I) is a key enzyme that regulates the distributio
98  the stable or transient localization of the ST6Gal I isoforms in the Golgi.
99                                    These two ST6Gal I isoforms were used to explore the role of the b
100                       We have found that the ST6Gal-I isoforms are phosphorylated on luminal Ser and
101                                              ST6Gal-I KD also alters mRNA expression of key gemcitabi
102                                              ST6Gal-I KD in S2-013 cells increases gemcitabine-mediat
103                                        Using ST6Gal-I knockdown and forced overexpression colon carci
104 ing pancreatic and ovarian cancer cells with ST6Gal-I knockdown or overexpression, we determined that
105 ubcutaneous tumor formation was inhibited by ST6Gal-I knockdown, whereas in a chemically induced tumo
106 of splenic and BM B cell subsets in CD22 and ST6Gal-I knockout mice revealed that ST6Gal-I-generated
107  isoforms of the alpha2,6-sialyltransferase (ST6Gal I) leads to differences in their trafficking, pro
108 , we find that serum-starved cells with high ST6Gal-I levels exhibit increased activation of prosurvi
109 nded TNF treatment (6-24 h), cells with high ST6Gal-I levels exhibited resistance to TNF-induced apop
110 ine-resistant MiaPaCa-2 cells display higher ST6Gal-I levels than treatment-naive cells along with a
111                             In normal colon, ST6Gal-I localized selectively to the base of crypts, wh
112  metastasis and poor survival, and therefore ST6Gal-I-mediated hypersialylation likely plays a role i
113  transfer purified B cells from wild-type or ST6Gal I(-/-) mice into B cell-deficient (microMT(-/-))
114                 At later memory time points, ST6Gal I(-/-) mice show comparable numbers of IgG influe
115 ntiviral B cell immune response, we infected ST6Gal I(-/-) mice with influenza A/HKx31.
116                                              ST6Gal-I mRNA has been reported to be upregulated in hum
117 versed collagen binding back to the level of ST6Gal-I nonexpressors, confirming that alpha2-6 sialyla
118                                   Tissues of ST6Gal-I null mice showed minimal binding of an alpha2-6
119                             Up-regulation of ST6Gal-I occurs in many cancers, including colon carcino
120 ith TRAIL, implicating a selective effect of ST6Gal-I on the Fas receptor.
121 g that O-acetylation is not induced when the ST6Gal I or ST8Sia I cDNAs are overexpressed in SV40 T a
122 umor initiation model, mice with conditional ST6Gal-I overexpression exhibited enhanced tumorigenesis
123 arian and pancreatic cancer cell models with ST6Gal-I overexpression or knockdown, we find that serum
124           This suggests that the bulk of the ST6Gal-I phosphorylation is occurring in the Golgi.
125                                     Elevated ST6Gal-I positively correlates with metastasis and poor
126                          Additionally, KD of ST6Gal-I potentiates gemcitabine-induced DNA damage as m
127                                  Because the ST6Gal I preferentially utilizes N-glycans as acceptor s
128       Collectively, our results suggest that ST6Gal-I promotes tumorigenesis and may serve as a regul
129                    Here, we show upregulated ST6Gal-I protein in several epithelial cancers, includin
130 s has limited immunochemical analysis of the ST6Gal-I protein.
131 , S2-LM7AA, and S2-013, exhibit up-regulated ST6Gal-I relative to parental Suit2 cells.
132                     Protein glycosylation by ST6Gal-I restricts access of antigen receptors and Shp-1
133                         BACE1 up-regulation, ST6Gal-I shedding, beta1 hyposialylation, and alpha4beta
134 th suppressed BCR signaling, B cells lacking ST6Gal I showed a net redistribution of the BCR to clath
135 her neuraminidase treatment or expression of ST6Gal-I shRNA markedly enhanced TNFalpha-mediated apopt
136 ged by exogenously administering recombinant ST6Gal I sialyltransferase and azide-modified CMP-Neu5Ac
137 duces a down-regulation in expression of the ST6Gal I sialyltransferase.
138                                          The ST6Gal-I sialyltransferase adds an alpha2-6-linked siali
139         Here, we report a novel role for the ST6Gal-I sialyltransferase in gemcitabine resistance.
140                                          The ST6Gal-I sialyltransferase produces Siglec ligands for t
141 onocyte/macrophage lineage down-regulate the ST6Gal-I sialyltransferase via a protein kinase C/Ras/ER
142            In this study, we report that the ST6Gal-I sialyltransferase, an enzyme up-regulated in nu
143 alylation of the TNFR1 death receptor by the ST6Gal-I sialyltransferase.
144 ds, a carbohydrate modification added by the ST6Gal-I sialyltransferase.
145 ion of the CD22 glycan ligand(s) produced by ST6Gal-I sialyltransferase.
146 a-galactoside alpha-2,6-sialyltransferase 1 (ST6Gal-I) sialyltransferase, which is up-regulated in nu
147                  Although both ST3Gal-IV and ST6Gal-I sialyltransferases mask galactose linkages impl
148                            Expression of the ST6Gal I specifically resulted in increased sialylation
149 entify the death receptor, Fas (CD95), as an ST6Gal-I substrate, and show that alpha2-6 sialylation o
150             B cells deficient in the enzyme (ST6Gal I) that forms the CD22 ligand show suppressed BCR
151 as-dependent alteration in the expression of ST6Gal I, the enzyme that adds alpha2-6-linked sialic ac
152 pha2-6 sialylation and increased activity of ST6Gal-I, the Golgi glycosyltransferase that creates alp
153  that that uses alpha-2,6-sialyltransferase (ST6Gal-I) to enzymatically add 13C-N-acetylneuraminic ac
154                             Furthermore, the ST6Gal I transfectants produced no intracranial tumors i
155 Galbeta1,4GlcNAc alpha2,6-sialyltransferase (ST6Gal I) transfectants were made to replace the endogen
156 d vector-transfected control cells in vitro, ST6Gal I transfection abolished invasion in vitro and in
157 mice in comparison with animals deficient in ST6Gal-I (transfers alpha2-6-linked sialic acid to Galbe
158 FR1 sialylation, we generated overexpressing ST6Gal-I transgenic mice.
159                                     Notably, ST6Gal-I upregulation in cancer cells conferred hallmark
160 r previous study the larger L-sialylmotif of ST6Gal I was analyzed by site-directed mutagenesis, whic
161                The catalytic domain from rat ST6Gal-I was expressed in mammalian HEK293 cells.
162                                              ST6Gal-I was highly expressed in induced pluripotent ste
163 sion due to the various 13C-NeuAc adducts on ST6Gal-I was observed in a 3D experiment correlating 1H-
164 uced by the human alpha2-6 sialyltransferase ST6Gal-I, were identified as potent anti-inflammatory me
165                      The glycosyltransferase ST6Gal-I, which adds alpha2-6-linked sialic acids to sub
166 ialyltransferases ST3Gal-III, ST3Gal-IV, and ST6Gal-I, which together are responsible for addition of
167 s, we investigated further an association of ST6Gal-I with cancer stem cells (CSC).
168 ed removal of the native NeuAc residues from ST6Gal-I with neuraminidase, separation of the neuramind

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