ライフサイエンスコーパス: Glc

1 Glc also antagonizes BR reset but acts independently of

2 Glc and BR can promote LR emergence at lower concentrati

3 Glc could also regulate several genes involved in BR met

4 Glc could regulate the transcript level of 72% of BR-reg

5 Glc may interact with BR via a hexokinase1 (HXK1)-mediat

6 Glc-supplemented cells exhibited a marked reduction in l

7 tingly, the galactose-masked glycoform Gal(1)Glc(1)Man(9)GlcNAc(2)-RNase also showed significant affi

8 is of a selectively modified glycoform Gal(1)Glc(1)Man(9)GlcNAc(2)-RNase was accomplished by chemical

9 Feeding experiments using (1-13C)Glc followed by analysis of labeling patterns by 13C-NMR

10 Seedling transfer to plates with 2% Glc plus ACC mimics the high-Glc effect in the HKL1 over

11 ctures revealed the disaccharide Rha-(1-->3)-Glc as a minimal epitope.

12 de repeating unit as well as the Rha-(1-->3)-Glc disaccharide are promising novel vaccine candidates

13 A CRM197-Rha-(1-->3)-Glc disaccharide conjugate was able to elicit antibodies

14 ere observed among all five substrates (1-3, Glc 1P, and Man 1P) for either enzyme-catalyzed reaction

15 lactose [Gal-beta(1 --> 6)-Gal-beta(1 --> 4)-Glc].

16 plates with normal medium to plates with 6% Glc.

17 ial dextran) which also contain alpha-(1,3,6)Glc branch points.

18 --> 6)-Gal], allolactose [Gal-beta(1 --> 6)-Glc] and 6'-O-beta-galactosyl-lactose [Gal-beta(1 --> 6)

19 type seedlings transferred to plates with 9% Glc.

20 s (C1alpha, C1beta, C2, C3, C4, and C6) of a Glc-Pt.

21 tive oxygen species, which in turn activated Glc-6-PD.

22 ha) regulates stress tolerance by activating Glc-6-phosphate dehydrogenase (G6PD), which is essential

23 catalyzes the synthesis of ADP-glucose (ADP-Glc) from Glc-1-phosphate (G-1-P) and ATP.

24 When expressed individually GlgC had ADP-Glc PPase activity, whereas GlgD was inactive.

25 Results indicate that S. mutans ADP-Glc PPase is an allosteric regulatory enzyme exhibiting

26 It is proposed that the accumulation of ADP-Glc in the ss3/ss4 mutant sequesters a large part of the

27 ucomutase (pgm1) or the small subunit of ADP-Glc pyrophosphorylase (aps1), largely restored photosynt

28 putative ADP-glucose pyrophosphorylases (ADP-Glc PPase), a key enzyme for glycogen synthesis in most

29 Restricting ADP-Glc synthesis, by introducing mutations in the plastidia

30 r starch deficient in all plant tissues (ADP-Glc-pyrophosphorylase [ADGase]) or retain starch accumul

31 sient expression of a Pseudomonas aeruginosa Glc(NAc) C4-epimerase and a human polypeptide GalNAc-tra

32 ha-Fuc2(SO3)1-->3-alpha-Glc4(SO3)1-->3-alpha-Glc-->4-li nked to the central alpha-Glc units.

33 3-alpha-Glc-->4-li nked to the central alpha-Glc units.

34 ished endo-alpha-mannosidase inhibitor alpha-Glc-1,3-deoxymannonojirimycin and a newly developed inhi

35 mycin and a newly developed inhibitor, alpha-Glc-1,3-isofagomine, and with the reducing-end product a

36 and MCL promastigotes were alpha-Man, alpha-Glc, and alpha-Gal.

37 Using the bespoke substrate alpha-Glc-1,3-alpha-Man fluoride, the enzyme was shown to act

38 Both BR and Glc coregulate a large number of genes involved in abiot

39 terdependence/overlap occurs between BR- and Glc-regulated gene expression as well as physiological r

40 Experiments with (13)C6 labelled Gal and Glc showed that both monosaccharides act as acceptor sub

41 s indicated increased succinate, malate, and Glc-6-P and decreased Fru-1,6-bisphosphate, illustrating

42 tiating the idea that glucose metabolism and Glc-6-PD play roles in the response of PA to hypoxia.

43 ls lacking NR1D1, fails to inhibit PEPCK and Glc-6-Pase gene expression; and stimulates higher hepati

44 oA-IV suppresses the expression of PEPCK and Glc-6-Pase in hepatocytes; decreases hepatic glucose pro

45 d by physiological concentrations of Suc and Glc and in pap1-D, an activation-tagged line, indicating

46 te cross talk between the normal antagonists Glc and ethylene.

47 Enzymatic cleavage of authentic Glc(1/3)Man(9)GlcNAc(2) yields Glc(1/3)-Man.

48 ng units composed of the following: -4)-beta-Glc-(1-3)-Sug-(1-4)-beta-GlcA-(1- | beta-GlcNAc-(1-2) Su

49 rminal beta-glucosylserine residue, Ser(beta-Glc)NH2, a modification that has previously been shown t

50 cated a positive linear relationship between Glc-6-PD activity and HPV.

51 insulin-glucagon system for regulating blood Glc levels in animals.

52 e Fru, while under nitrogen starvation, both Glc and Fru, but not Suc, were less abundant.

53 , C-GlcNAc Ser, has been prepared from the C-Glc Ser by a double inversion strategy using azide to in

54 The C-Glc Ser was available by a ring-closing metathesis and h

55 The alpha- and beta-anomers of the C1-Glc-Pt also differ significantly in their cellular uptak

56 ently compared to the others, whereas the C3-Glc-Pt (3) is taken up least efficiently.

57 lucose-1-phosphate cytidylyltransferase, CDP-Glc 4,6-dehydratase, NADH-dependent SAM:C-methyltransfer

58 For uptake into cells, Glc-Pt 1 exploits both glucose and organic cation transp

59 e phenotypes occur independently of cellular Glc signaling activities, we have tested whether HKL1 mi

60 onally designed glucose-platinum conjugates (Glc-Pts) were synthesized and their biological activitie

61 cal activity of glucose-platinum conjugates (Glc-Pts).

62 stingly, the protein has a largely conserved Glc-binding domain, and protein overexpression was shown

63 matic analysis of myelin proteins and CSF114(Glc), which led to the identification of five sequences.

64 , showing a higher homology with both CSF114(Glc) and the five sequences selected using the bioinform

65 We previously reported that CSF114(Glc) detects diagnostic autoantibodies in multiple scler

66 higher antibody titers as compared to CSF114(Glc).

67 4)-alpha-Neu5Ac-(2 -->)n and (--> 6)-alpha-D-Glc-(1 --> 4)-alpha-Neu5Ac-(2 -->)n, respectively.

68 pha-Neu5Ac-(2-->)n in NmW and (-->6)-alpha-d-Glc-(1-->4)-alpha-Neu5Ac-(2-->)n in NmY.

69 3-O-beta-d-Glc hederagenin strongly deterred feeding, while 3-O-bet

70 strongly deterred feeding, while 3-O-beta-d-Glc oleanolic acid only had a minor effect, showing that

71 aride unit alpha-D-PerNAc-alpha-l-Fuc-beta-D-Glc-alpha-D-GalNAc, preassembled on undecaprenyl pyropho

72 eu5Ac-(2 --> 3)]-beta-D-Gal-(1 --> 4)-beta-D-Glc-ceramide (GM1), and between a recombinant fragment o

73 hibits hepatic gluconeogenesis by decreasing Glc-6-Pase and PEPCK gene expression through NR1D1.

74 bution of glucose-6-phosphate dehydrogenase (Glc-6-PD), an important regulator of NADPH redox and pro

75 f the 8-O-methylated benzoxazinoids, DIM2BOA-Glc and HDM2BOA-Glc.

76 e start codon of Bx13 and lacks both DIM2BOA-Glc and HDM2BOA-Glc, and Il14H, which has an inactive Bx

77 thyltransferase (BX14) that converts DIM2BOA-Glc to HDM2BOA-Glc.

78 nd Oh43 revealed that the absence of DIM2BOA-Glc and HDM2BOA-Glc does not alter the constitutive accu

79 rformance increased, suggesting that DIM2BOA-Glc and/or HDM2BOA-Glc provide specific protection again

80 TRIMBOA-Glc is then converted to DIM2BOA-Glc by a previously described O-methyltransferase BX7.

81 yltransferases (Bx10a-c) that convert DIMBOA-Glc to HDMBOA-Glc.

82 thoxy-1,4-benzoxazin-3-one glucoside (DIMBOA-Glc).

83 on those with high HDMBOA-Glc and low DIMBOA-Glc.

84 X13) that catalyzes the conversion of DIMBOA-Glc into a new benzoxazinoid intermediate (TRIMBOA-Glc)

85 activity and the resulting decline of DIMBOA-Glc upon methylation to HDMBOA-Glc were associated with

86 -Glc was more toxic to R. maidis than DIMBOA-Glc in vitro, BX10c activity and the resulting decline o

87 The disaccharides Glc-(1-->3)-Hep4P Hep-(1-->3)-Hep4P and Hep-(1-->7)-Hep4

88 ected frame-shifted thiodisaccharide donors, Glc-GlcA and GlcA-Glc, were compared.

89 complete absence of structures for any EIIA(Glc)-transporter complexes.

90 ains lacking EI, Hpr, or the associated EIIA(Glc) protein produced less cholera toxin (CT) and had a

91 A crystal structure of Escherichia coli EIIA(Glc) in complex with the maltose transporter, an ATP-bin

92 mbrane anchor to increase the effective EIIA(Glc) concentration at the membrane.

93 volve the glucose-specific enzyme EIIA (EIIA(Glc)) and two nitrogen-specific EIIA homologs, EIIA(Ntr1

94 How EIIA(Glc) is targeted to the membrane, how it interacts with

95 phosphotransferase system, enzyme IIA (EIIA(Glc)).

96 itory concentrations of the full-length EIIA(Glc) and an amino-terminal truncation mutant differ by 6

97 ds together with the N-terminal tail of EIIA(Glc) are essential for the high affinity binding of the

98 Only the unphosphorylated form of EIIA(Glc) bound to CsrD in vitro and was capable of activatin

99 ferred carbon source via the binding of EIIA(Glc) of the glucose transport system to the GGDEF-EAL do

100 l of how the central regulatory protein EIIA(Glc) allosterically inhibits maltose uptake in E. coli.

101 The signal-transducing protein EIIA(Glc) belongs to the phosphoenolpyruvate carbohydrate pho

102 In its dephosphorylated state, EIIA(Glc) is a negative regulator for several permeases, incl

103 ical cross-linking, we demonstrate that EIIA(Glc) binds to the MalK dimer, interacting with both the

104 ection of the ATPase cycle reveals that EIIA(Glc) does not affect the binding of ATP but rather inhib

105 Here, we show that EIIA(Glc) of the glucose-specific PTS system is also required

106 sponsible for cAMP generation, that the EIIA(Glc) component of glucose transport could enhance cAMP p

107 The structure shows that two EIIA(Glc) molecules bind to the cytoplasmic ATPase subunits,

108 It is known that unphosphorylated EIIA(Glc) binds to and inhibits a variety of transporters whe

109 main, and an important new way in which EIIA(Glc) shapes global regulatory circuitry in response to n

110 and the glucose-specific enzyme IIBC (EIIBC(Glc)) in defined media that lack PTS substrates.

111 present, the unphosphorylated form of EIIBC(Glc) sequesters Mlc to the cell membrane, preventing its

112 encodes the major glucose transporter EIICB(Glc).

113 Finally, Glc-bleached SSB01 cells appeared unable to efficiently

114 in signaling mutants that were defective for Glc-induced LR production.

115 te pathway (OPPP) metabolism is required for Glc-mediated NITRATE TRANSPORTER2.1 (NRT2.1) expression.

116 completely depolymerize tamarind XG to free Glc or Xyl, respectively.

117 are formed from acceptor reactions with free Glc and not by rearrangement of Glc in the active site.

118 the synthesis of ADP-glucose (ADP-Glc) from Glc-1-phosphate (G-1-P) and ATP.

119 on of the biosynthetic pathways leading from Glc to anthocyanins.

120 ity were significantly reduced in lungs from Glc-6-PD(mut(-/-)) mice, and there was a corresponding r

121 epI, whereas a mutant that expressed Gal-Gal-Glc-HepI fully resisted killing (>100% survival).

122 enotypes of the lactose-HepI and the Gal-Gal-Glc-HepI LOS structures were recapitulated with phase va

123 Despite lack of killing of the Gal-Gal-Glc-HepI mutants, mAb 2C7 deposited sufficient C3 on the

124 Mutants that elaborated 4- (Gal-GlcNAc-Gal-Glc-HepI) and 5-glycan (GalNAc-Gal-GlcNAc-Gal-Glc-HepI)

125 lc-HepI) and 5-glycan (GalNAc-Gal-GlcNAc-Gal-Glc-HepI) structures displayed intermediate phenotypes (

126 isteria monocytogenes this glycolipid is Gal-Glc-DAG or Gal-Ptd-6Glc-DAG.

127 2C7 of a mutant that expressed lactose (Gal-Glc) from HepI, whereas a mutant that expressed Gal-Gal-

128 flours were, on average, Rha:Ara:Xyl:Man:Gal:Glc:GalA in a 3:32:2:13:11:20:19 M ratio, with varying G

129 Our analyses indicate the GalNAc/Glc polymer and glycine are exported by the ExoA-I syste

130 ion, catalyzing the transfer of GlcNAc, Glc, Glc and GlcNAc residues to the protein backbone sequenti

131 ion, catalyzing the transfer of GlcNAc, Glc, Glc, and GlcNAc residues to the protein backbone sequent

132 d thiodisaccharide donors, Glc-GlcA and GlcA-Glc, were compared.

133 sylation, catalyzing the transfer of GlcNAc, Glc, Glc and GlcNAc residues to the protein backbone seq

134 sylation, catalyzing the transfer of GlcNAc, Glc, Glc, and GlcNAc residues to the protein backbone se

135 Glucose (Glc) plays a fundamental role in regulating lateral root

136 accumulates over 170 times more ADP-glucose (Glc) than wild-type plants.

137 ied the interactions of nitrate and glucose (Glc) on gene expression, nitrate transport, and growth u

138 Brassinosteroid (BR) and glucose (Glc) regulate many common responses in plants.

139 N-acetylgalactosamine (GalNAc), and glucose (Glc), using gas chromatograph mass spectrometry (GC-MS),

140 standing performance for enzymeless glucose (Glc) sensing in alkaline media with high sensitivity (31

141 iana) Hexokinase-Like1 (HKL1) lacks glucose (Glc) phosphorylation activity and has been shown to act

142 We show that 1-4-linked glucose (Glc) is likely a minor component of the spore coat with

143 1 transported sucrose (Suc) but not glucose (Glc).

144 ulated millimolar concentrations of glucose (Glc) and fructose (Fru).

145 evealed that kefiran is composed of glucose (Glc) and galactose (Gal) in a relative molar ratio of 1.

146 re hypersensitive to high levels of glucose (Glc) but responded normally to high salinity and osmotic

147 N, WbdO and WbdP) and they transfer glucose (Glc), L-fucose (L-Fuc) and N-acetylperosamine (PerNAc) o

148 cuole-located carrier, transporting glucose (Glc), fructose (Fru), and sucrose (Suc) after heterologo

149 nin, ethylene) and nutrient status (glucose [Glc], sucrose).

150 e three-branched N-glycan precursor [glucose(Glc)](3)(Man)(9)[N-acetylglucosamine(GlcNAc)](2).

151 , as indicated by the accumulation of a GroP-Glc(2) -DAG glycolipid.

152 that the absence of DIM2BOA-Glc and HDM2BOA-Glc does not alter the constitutive accumulation or degl

153 Bx13 and lacks both DIM2BOA-Glc and HDM2BOA-Glc, and Il14H, which has an inactive Bx14 allele and la

154 ated benzoxazinoids, DIM2BOA-Glc and HDM2BOA-Glc.

155 as an inactive Bx14 allele and lacks HDM2BOA-Glc in leaves.

156 , suggesting that DIM2BOA-Glc and/or HDM2BOA-Glc provide specific protection against phloem feeding i

157 (BX14) that converts DIM2BOA-Glc to HDM2BOA-Glc.

158 Although HDMBOA-Glc was more toxic to R. maidis than DIMBOA-Glc in vitro

159 thoxy-1,4-benzoxazin-3-one glucoside (HDMBOA-Glc) and low levels of 2,4-dihydroxy-7-methoxy-1,4-benzo

160 root-derived benzoxazinoid glucosides HDMBOA-Glc and MBOA-Glc.

161 duced more progeny on those with high HDMBOA-Glc and low DIMBOA-Glc.

162 The larvae can hydrolyze HDMBOA-Glc, but not MBOA-Glc, to produce toxic MBOA upon predat

163 Variation in HDMBOA-Glc production was attributed to a natural CACTA family

164 tivates Bx10c in maize lines with low HDMBOA-Glc accumulation.

165 ine of DIMBOA-Glc upon methylation to HDMBOA-Glc were associated with reduced callose deposition as a

166 (Bx10a-c) that convert DIMBOA-Glc to HDMBOA-Glc.

167 While HDMBOA-Glc and MBOA reduce the growth and infectivity of both t

168 abi4, scr became much more tolerant of high Glc.

169 air phenotype associated with growth on high Glc medium that occurs prominently in HKL1 overexpressio

170 plates with 2% Glc plus ACC mimics the high-Glc effect in the HKL1 overexpression line but not in gi

171 IIA(Glc) binding to MelB(St) in the absence or presence of m

172 their thermodynamic response to binding IIA(Glc).

173 ity of LacY are subject to regulation by IIA(Glc) (inducer exclusion).

174 duced-fit mechanism that is inhibited by IIA(Glc) binding.

175 e mechanism of the inhibition of LacY by IIA(Glc) elucidated by ITC differs from the inhibition of me

176 By suppressing conformational dynamics, IIA(Glc) blocks inducer entry into cells and favors constitu

177 ; in addition, thermodynamic features of IIA(Glc) binding to other proteins are also unknown.

178 The phosphotransfer protein IIA(Glc) of the bacterial phosphoenolpyruvate:carbohydrate p

179 bacteria, the phosphotransferase protein IIA(Glc) plays a key regulatory role in catabolite repressio

180 The studies show that IIA(Glc) binds to LacY with a Kd of about 5 muM and a stoich

181 ine-specific cross-linking, we show that IIA(Glc) directly binds to MelB of Salmonella typhimurium (M

182 consistent with the interpretation that IIA(Glc) inhibits the induced fit process and restricts the

183 We further found that the IIA(Glc)-bound MelB(St) exhibits a decreased binding affinit

184 report the thermodynamic features of the IIA(Glc)-LacY interaction as measured by isothermal titratio

185 s one among several permeases subject to IIA(Glc) regulation.

186 Upon IIA(Glc) binding, the conformational entropy of LacY is rest

187 However, the altered carbon metabolism in Glc-supplemented cells was correlated with modest altera

188 two proteins likely form a critical node in Glc signaling that mediates overlapping, but also distin

189 hat HKL1 and HXK1 have differential roles in Glc-dependent repression of some ethylene biosynthesis g

190 f the models for some metabolites, including Glc-6-P, Fru-6-P, malate, fumarate, Xyl, and ribose.

191 Starch is a water-insoluble, Glc-based biopolymer that is used for energy storage and

192 een the glucose derivative-modified insulin (Glc-Insulin) and glucose transporters on erythrocytes (o

193 ferences in sugar accumulation, such as less Glc, Fru, and Suc at the end of the night.

194 nked Gal, (1-->4)-linked Gal, (1-->4)-linked Glc and (1-->2,6)-linked Gal, with a branch attached to

195 firan possessed a backbone of (1-->6)-linked Glc, (1-->3)-linked Gal, (1-->4)-linked Gal, (1-->4)-lin

196 ssigned as Man8 glycan, was found to be Man7+Glc glycan as its 1,3 branch containing three mannoses a

197 found that the newly identified "Man8" (Man7+Glc) was also present in different batches and in some c

198 MBOA-Glc is produced by D. virgifera through stabilization of

199 benzoxazinoid glucosides HDMBOA-Glc and MBOA-Glc.

200 of both the nematodes and the bacteria, MBOA-Glc repels infective juvenile nematodes.

201 arvae can hydrolyze HDMBOA-Glc, but not MBOA-Glc, to produce toxic MBOA upon predator attack.

202 pair the Muller cell's ability to metabolize Glc.

203 1brassinosteroid insensitive1 double mutant, Glc-induced LR production/emergence was severely reduced

204 antibodies specific to a gluco-asparagine (N-Glc) glycopeptide, CSF114(N-Glc), were identified in ser

205 co-asparagine (N-Glc) glycopeptide, CSF114(N-Glc), were identified in sera of an MS patient subpopula

206 expressing cell-surface adhesins including N-Glc, to establish a connection between H. influenzae inf

207 Consistent with the abundance of Glc and Fru in the gland prior to Nostoc colonization, g

208 paired growth, a decrease in the activity of Glc-6-P dehydrogenase, a decrease of the transcript abun

209 Analysis of Glc and BR sensitivity in mutants defective in auxin res

210 Application of Glc, Fru, or Suc, as well as cold, osmotic stress, or lo

211 STANT2,3 and SOLITARY ROOT act downstream of Glc and BR.

212 nosteroid (BR) signaling works downstream of Glc in controlling LR production/emergence in Arabidopsi

213 BR signaling works downstream of Glc signaling in regulating LR production, as in the glu

214 gar levels, points to a superior function of Glc and Suc for frost tolerance.

215 Inhibition of Glc-6-PD decreased Ca(2+) sensitivity to the myofilament

216 A unifying and hierarchical model of Glc and hormone signaling interplay is proposed.

217 Presence of Glc along with BR in medium could affect BR induction/re

218 ns with free Glc and not by rearrangement of Glc in the active site.

219 The transcriptional regulation of Glc-6-Pase and phosphoenolpyruvate carboxykinase (PEPCK)

220 iporter GPT1 as the putative translocator of Glc-6-phosphate for starch biosynthesis in reproductive

221 with lactose plus the monosaccharides Gal or Glc resulted in altered GOS profiles.

222 sosteric alpha-d-glucopyranosyl 1-phosphate (Glc 1P) analogues have been synthesized.

223 sterically activated by glucose 6-phosphate (Glc-6-P) and adenosine monophosphate (AMP).

224 Physiologically, Glc and BR interact to regulate hypocotyl elongation gro

225 udies included incorporation of radiolabeled Glc, linkage analysis, and imaging of cellulose microfib

226 Finally, regression analysis relating Glc-6-PD activity and the NADPH-to-NADP(+) ratio to the

227 o a rhodamine fluorophore, which affords RhB-Glc-Ent, it can selectively label Gram-negative bacteria

228 Our results suggest that the RhB-Glc-Ent probe is sensitive not only to the bacterial str

229 nalogue 6 (Tyr-d-Ala-Gly-Phe-Nle-Pro-Leu-Ser(Glc)-Trp-NH-3',5'-Bzl(CF(3))(2)) was found to have effec

230 Incorporation of Ser(Glc) into various positions of TY027 gave analogues with

231 derivative, O-beta-glycosylated serine (Ser(Glc)) was introduced into TY027 (Tyr-d-Ala-Gly-Phe-Met-P

232 Silencing Glc-6-PD expression in PA using a targeted small interfe

233 Similarly, Glc-6-PD expression and activity were significantly redu

234 idespread occurrence of the glycan structure Glc(alpha1-2)Gal linked to hydroxylysine in animals, the

235 The results reveal that C2-substituted Glc-Pt 2 has the highest GLUT1-specific internalization,

236 The C1alpha- and C2-substituted Glc-Pts (1alpha and 2) accumulate in cancer cells most e

237 c efficiency (V(max)/K(m)) for the substrate Glc-1-P.

238 accumulated in gland tissue, namely sucrose, Glc, and Fru, inhibited hormogonia differentiation and e

239 The endogenous levels of sucrose, Glc, and fructose were also elevated in shr and scr.

240 homologs with a >15-fold preference for TDP-Glc over UDP-Glc.

241 roduce the same nascent tetradecasaccharide (Glc(3)Man(9)GlcNAc(2)), heterogeneity is introduced into

242 Based on these findings, we propose that Glc-6-PD and NADPH redox are crucially involved in the m

243 We also show that Glc stimulates NRT2.1 protein levels and transport activ

244 Here we show that Glc supplementation of SSB01 cultures causes a loss of p

245 on is not influenced by gin2-1, showing that Glc does not influence NRT2.1 expression through nitrate

246 in response/signaling further suggested that Glc and BR signals may converge at S-phase kinase-associ

247 The Glc-GlcA disaccharide, featuring the glucuronic acid don

248 The Glc-Pts, 1-3, exhibit high levels of cytotoxicity toward

249 ly reduced numbers of emerged LRs at all the Glc concentrations tested.

250 nsitive1 (BRI1) is epistatic to HXK1, as the Glc insensitive2bri1-6 double mutant displayed severe de

251 l galactose by a beta-galactosidase gave the Glc(1)Man(9)GlcNAc(2)-RNase glycoform in excellent yield

252 bolism and translocation, and identified the Glc-6-phosphate/phosphate antiporter GPT1 as the putativ

253 Increasing light flux could also mimic the Glc effect on LR production/emergence.

254 t of the spore coat with the majority of the Glc arising from contamination with extracellular polysa

255 discoveries revealing the importance of the Glc(3)Man(9)GlcNAc(2) C-branch in generating an ERAD sig

256 ocyclopropane-1-carboxylic acid (ACC) of the Glc-dependent developmental arrest of wild-type Arabidop

257 The GLUT1 specificity of the Glc-Pts was evaluated by determining the cellular uptake

258 target and cellular uptake mechanism of the Glc-Pts were elucidated.

259 No significant differences in uptake of the Glc-Pts were observed in non-cancerous RWPE2 cells.

260 RAD signal, the ebs3-1 mutation prevents the Glc(3)Man(9)GlcNAc(2) assembly and inhibits the ERAD of

261 SPR binding studies revealed that the Glc(1)Man(9)GlcNAc(2)-RNase had high affinity to lectin

262 d incorporating the SPE sensor for real-time Glc detection in human urine samples; the results obtain

263 ruitment of NR1D1 and activity by apoA-IV to Glc-6-Pase promoter was verified with ChIP and a lucifer

264 in Rft1-depleted cells (YG1137) relative to Glc(3)Man(9)GlcNAc(2)-P-P-Dol in wild type (SS328) cells

265 transferase, transferring GlcNAc residues to Glc-Glc-GlcNAc-modified Fap1.

266 syltransferase, transferring Glc residues to Glc-GlcNAc-modified Fap1.

267 in controlling LR production in response to Glc and BR.

268 ng, but also distinct, cellular responses to Glc and ethylene treatments.

269 those of scr, it was much less sensitive to Glc.

270 GT-D-type glycosyltransferase, transferring Glc residues to Glc-GlcNAc-modified Fap1.

271 TRIMBOA-Glc is then converted to DIM2BOA-Glc by a previously des

272 to a new benzoxazinoid intermediate (TRIMBOA-Glc) by an uncommon reaction involving a hydroxylation a

273 (1-->7)-Hep4P and the branched trisaccharide Glc-(1-->3)-[Hep-(1-->7)]-Hep4P, respectively, have been

274 UDP-Glc also stimulated keratinocyte migration, proliferatio

275 Specificity of binding to UDP and UDP-Glc indicates a properly folded protein, and binding kin

276 ive binding orientations of UDP-Galp and UDP-Glc were compared using saturation transfer difference N

277 cked the induction of HAS2 expression by UDP-Glc, the latter inhibitor suggesting that the signaling

278 ascent proteins and the glucose added by UDP-Glc:glycoprotein glucosyltransferase.

279 phenylalanine (Phe-391) in UGT3A2 favors UDP-Glc use.

280 d (UDP-GlcA) and display specificity for UDP-Glc.

281 ate (GCP) was proposed to be formed from UDP-Glc breakdown and subsequently transferred, thus providi

282 in complex with natural donors UDP-Gal, UDP-Glc and, in an attempt to overcome one of the common pro

283 from keratinocytes and that UDP-glucose (UDP-Glc) added into keratinocyte cultures induced a specific

284 e the conversion of UDP-alpha-d-glucose (UDP-Glc) to the key metabolic precursor UDP-alpha-d-glucuron

285 samine (UDP-GlcNAc) but not UDP-glucose (UDP-Glc).

286 c but allows a more optimal alignment of UDP-Glc for sugar donation.

287 NMR studies of UDP-Glc hydrolysis by yeast glycogen synthase were used to v

288 h a >15-fold preference for TDP-Glc over UDP-Glc.

289 L-8 expression, supporting a notion that UDP-Glc signals for epidermal inflammation, enhanced hyaluro

290 aliana) lines carrying insertions in the UDP-Glc:sterol glucosyltransferase genes, UGT80A2 and UGT80B

291 as preferred sugar donor and UGT3A2 uses UDP-Glc.

292 n UGT3A1 enhances its ability to utilize UDP-Glc and completely inhibits its ability to use UDP-GlcNA

293 ote seedling tolerance to exogenous 6% (w/v) Glc.

294 n a 3:32:2:13:11:20:19 M ratio, with varying Glc:GalA ratios.

295 ers coated with RBC membrane and loaded with Glc-Insulin.

296 ally or heterotrophically when supplied with Glc, a metabolite normally transferred from the alga to

297 d to O-2 of Gal residues and terminated with Glc residues.

298 ived from OPPP metabolism can, together with Glc, directly stimulate high levels of NRT2.1 expression

299 ently elongated to the trisaccharide Xyl-Xyl-Glc.

300 of authentic Glc(1/3)Man(9)GlcNAc(2) yields Glc(1/3)-Man.