ライフサイエンスコーパス: sulfate group

1 ient to shield the charge contributed by the sulfate group.

2 ndent on the positioning of at least one 6-O-sulfate group.

3 ted di-, tri-, and pentasaccharides with one sulfate group.

4 e residue and the attachment position of the sulfate group.

5 s positioned to recognize the substrate beta-sulfate group.

6 ttranslationally modified by the addition of sulfate groups.

7 ic oligosaccharides as well as phosphate and sulfate groups.

8 2-O-sulfated iduronate residues, but no 6-O-sulfate groups.

9 in chains that lack their N-, C6-O-, or C2-O-sulfate groups.

10 that binding is specific to the presence of sulfate groups.

11 onal coordination of the ammonium across the sulfate groups.

12 ose containing a combination of 2-O- and 6-O-sulfate groups.

13 eived neither cobra venom factor nor dextran sulfate (group 1), there was rapid destruction of islets

14 gnificantly less frequently in the magnesium sulfate group (1.9% vs. 3.5%; relative risk, 0.55; 95% C

15 resolution of IDA was higher in the ferrous sulfate group (29% vs 6%; P = .04).

16 59 completed the trial (28 [70%] in ferrous sulfate group; 31 [78%] in iron polysaccharide complex g

17 methoxy (1), hydroxy (2), carbamate (3), or sulfate groups (4).

18 n the iron complex group than in the ferrous sulfate group (58% vs 35%, respectively; P = .04).

19 lfation pattern (statistical distribution of sulfate groups along a chain), ionic strength, CS intrin

20 ee of sulfation, but also the arrangement of sulfate groups along the GAG chain, plays a key role in

21 was most important, the 2-O-sulfate and 6-O-sulfate groups also contributed to neuregulin-1 binding

22 acquired HIV infections, 25 in the cellulose sulfate group and 16 in the placebo group, with an estim

23 school age was 14% (88/629) in the magnesium sulfate group and 18% (110/626) in the placebo group (ri

24 not significantly different in the magnesium sulfate group and the placebo group (11.3% and 11.7%, re

25 Salt bridges between the sulfate group and two lysine residues appear to compensa

26 ssays indicate that salt bridges between the sulfate group and two lysine residues compensate for the

27 , glycosulfopeptides permit the placement of sulfate groups and glycans of precise structure at defin

28 clearance depends on specific subclasses of sulfate groups and not on overall charge of the chains.

29 cid conditions without affecting the O- or N-sulfate groups and purified by reversed-phase high-perfo

30 pelling evidence that a specific subclass of sulfate groups, and not the overall charge of HS, permit

31 s controlled by sulfotransferases, which add sulfate groups, and sulfatases (Sulf), which remove 6-O-

32 r HLGAG oligosaccharides, provided that most sulfate groups are deprotonated.

33 d cell-surface GAG and, in particular, their sulfate groups are important in binding and modulation o

34 sulfate groups contribute to inhibition, 2-O-sulfate groups are less critical than either N- or 6-O-s

35 mportant for specificity and that at least 2 sulfate groups are required to cross-link spatially sepa

36 GAGs to mediate RSV infection, only certain sulfate groups are required.

37 is not crucial, and (c) additional negative sulfate groups are well tolerated in certain cases, such

38 ulfate, there is a very prominent role for N-sulfate groups, as opposed to a relatively small apparen

39 like hexasaccharide, bearing an additional O-sulfate group at the non-reducing end, which precludes b

40 The sulfate group at tyrosine 21 contributes substantially t

41 L-selectin-initiated cell adhesion; (b) the sulfate groups at C6 on the glucosamine residues play a

42 luronic acid) and 6S/4S/2S represent O-ester sulfate groups at C6/C4/C2 sites.

43 Modifications include the addition of sulfate groups at specific positions on sugar residues a

44 reas for AgaB oligosaccharides containing C6-sulfate groups at the -4, +1, and +3 positions are still

45 ransferases (3OSTs) catalyze the addition of sulfate groups at the 3-OH site of glucosamine in hepara

46 hat vGPCR is posttranslationally modified by sulfate groups at tyrosine residues within its N-termina

47 as modestly affected by the presence of a 17-sulfate group but severely impaired by the presence of a

48 ple charge interaction between the virus and sulfate groups but instead involves a specific GAG struc

49 SULF2 degrades HSPGs by removing 6-O sulfate groups, but had no previously known role in diab

50 nstrates that molecules completely devoid of sulfate groups can activate antithrombin effectively and

51 by a scaffold-based mechanism, in which the sulfate groups comprising GAGs interact primarily with T

52 asaccharide compositions based on acetyl and sulfate group content.

53 Although all N- and O-sulfate groups contribute to inhibition, 2-O-sulfate gro

54 th their preferential ability to co-ordinate sulfate groups), could form a single extended binding si

55 modified heparins lacking N-sulfate and 2-O-sulfate groups did not block very low density lipoprotei

56 sulfation reactions utilizing the universal sulfate group donor 3'-phosphoadenosine 5'-phosphosulfat

57 strogen sulfotransferase (EST) transfers the sulfate group from 3'-phosphoadenosine 5'-phosphosulfate

58 Sulfation is the transfer of a sulfate group from 3'-phosphoadenosine 5'-phosphosulfate

59 ylgalactosamine-4-sulfatase; ARSB) removes 4-sulfate groups from chondroitin-4-sulfate (C4S) and derm

60 lar endosulfatases, enzymes which remove 6-O sulfate groups from heparan sulfate chains, diminishes m

61 fatase-2 (SULF2), an enzyme that removes 6-O sulfate groups from heparan sulfate proteoglycans (HSPGs

62 tase and 6-O-sulfatase enzymes that cleave O-sulfate groups from specific locations of the HSGAG poly

63 ted endosulfatase Qsulf1 selectively removes sulfate groups from the 6-O position of sugars within th

64 ARSB is the enzyme that removes 4-sulfate groups from the non-reducing end of chondroitin

65 Recombinant human ARSG is able to cleave 3-O-sulfate groups from these residues as well as from an au

66 nzymatic removal of the non-reducing end 2-O-sulfate group had little effect on the 1:1 interaction w

67 revolutionized proteomics, the fragility of sulfate groups has limited its usefulness in the analysi

68 modified heparins reveals that 2-O- and 6-O-sulfate groups have potent bypass-inducing activity.

69 that the negatively charged sugar residue or sulfate group in gangliosides is one of the important si

70 er control values was detected in the copper sulfate group in terms of the aggregate modulus.

71 n EDD of GST, precluding localization of the sulfate group in that peptide.

72 on patterns depending on the position of the sulfate group in the heterocycle.

73 specific to the level and distribution of 4-sulfate groups in C4S.

74 sensitive to the content or arrangement of O-sulfate groups in heparan sulfate.

75 contacts between basic residues in gp120 and sulfate groups in proteoglycans, HIV-1 may exploit these

76 r the first time, the unique distribution of sulfate groups in the CS chains of placental CSPGs and t

77 The majority of the sulfate groups in the CSPGs are clustered in CS chain do

78 electively sulfated heparins indicate that O-sulfated groups in HS are critical for FGF10 signaling a

79 um ion complexation of HLGAGs stabilizes the sulfate groups, increases the relative abundances of bac

80 oups are less critical than either N- or 6-O-sulfate groups, indicating that inhibitory activity is d

81 x) blood group determinant, bringing several sulfate groups into close proximity and creating large n

82 Structure-function studies reveal that the sulfate group is an important determinant for efficient

83 sually a phosphate group and less commonly a sulfate group, leads to diverse structural and functiona

84 rs of 3,4-dihydroxyhex-5-enoic acid with the sulfate group located at the C-3 or C-4 position.

85 Only heparin chains lacking the N-sulfate group lost the ability to neutralize infection,

86 er of monosaccharide residues, acetylations, sulfate groups, multiple charges, and exchanges between

87 hazard ratio of infection for the cellulose sulfate group of 1.61 (P=0.13).

88 ulfo-Le(x), and forms a salt bridge with the sulfate group of 4'-sulfo-Le(x).

89 ts with both the iron-sulfur cluster and the sulfate group of adenosine 5'-phosphosulfate.

90 The 6-O-sulfate group of heparin plays a pivotal role in mediati

91 Whereas the N-sulfate group of heparin was most important, the 2-O-sul

92 In addition, the sulfate group of p-nitrocatechol sulfate was found to be

93 interaction, possibly communicating with the sulfate group of sulfatide by hydrogen bonding and/or sa

94 2-O-sulfate group of the I ring and the 6-O-sulfate group of the A ring are not.

95 l for site-specific binding, whereas the 2-O-sulfate group of the I ring and the 6-O-sulfate group of

96 etween this cationic amino acid and the core-sulfate group of the N-glycan is proposed to reduce mobi

97 n bonds either to the caboxylate or to the 4-sulfate groups of C4-S.

98 and galactose-6-sulfatase (GALNS) hydrolyze sulfate groups of CS.

99 th take advantage of binding of carboxyl and sulfate groups of GAGs to trivalent neodymium.

100 The sulfate groups of heparan sulfate- and chondroitin sulfa

101 m groups of FN-C/H II and carboxylate and/or sulfate groups of heparin.

102 e represented by peptide F-9 and the heparan sulfate groups of HSPG.

103 e ideally placed to receive the N-acetyl and sulfate groups of sulfated GalNAc residues of glycosamin

104 idues in positions 29, 42, and 77 in binding sulfate groups of the dp8 and dp10 forms of heparin.

105 ate-immobilized heparin, indicating that the sulfate groups of the glycosaminoglycan mediate p17 inte

106 bridging oxygen between the 5'-phosphate and sulfate groups of the PAPS molecule as is seen in the PA

107 In contrast, 6-sulfo sialyl Lex containing a sulfate group on the N-acetylglucosamine residue did not

108 In these interactions, the sulfate groups on C-2 were shown to interact more intens

109 The clustering of sulfate groups on heparin and its polymeric nature are e

110 inding depends on the amount and patterns of sulfate groups on HS, which are controlled by various HS

111 GSC number is sensitive to the levels of 6-O sulfate groups on HS.

112 An SPGG molecule containing approximately 10 sulfate groups on positions 2 through 6 of the pentagall

113 The installation of sulfate groups on the carbohydrate residues of glycoprot

114 rin on glypican binding also indicate that O-sulfate groups on the heparan sulfate chains play a crit

115 residues well placed to bind to clusters of sulfate groups on the high affinity dodecasaccharide.

116 are also modified by functionally important sulfate groups on their NH(2)-terminal tyrosines.

117 We propose that either the sulfate groups (or the sulfation pattern) at the reducin

118 ecasaccharides, only those with two or three sulfate groups per molecule showed maximum IRBC inhibiti

119 Replacement of the sterol hydroxyls with sulfate groups, prior to displacement with GSH, afforded

120 engineered heparan compounds containing 2-O-sulfate groups rescued Sdc1(-/-) mice from AILI by poten

121 ttributed to the presence of zirconium-bound sulfate groups structurally characterized using single-c

122 83k) and with limited changes in the cyclic sulfate group, such as 4,5-cyclic sulfite 87a/b.

123 More women in the magnesium sulfate group than in the nimodipine group needed hydral

124 The Methylocystis mbtins have a sulfate group that helps stabilize the Cu(I) forms, resu

125 molecules (500-900 Da) were also enriched in sulfate groups that appeared bound to UDOM.

126 t it is the negative charge, rather than the sulfate group, that confers inhibitory efficacy.

127 is challenging due to the lability of their sulfate groups, the high heterogeneity of modifications,

128 chimeric form of HNK-1ST was shown to add a sulfate group to a precursor, GlcAbeta1-->3Galbeta1-->4G

129 Introduction of an additional sulfate group to the 3-OH of residue H flanking a putati

130 ever, owing to their lability elimination of sulfate groups upon desorption/ionization is often encou

131 bin increased from 7.9 to 11.9 g/dL (ferrous sulfate group) vs 7.7 to 11.1 g/dL (iron complex group),

132 A glycolipid 3-sulfate group was essential for the T cell suppression,

133 Retention of sulfate groups was also observed in electron detachment

134 ted hepatocytes, whereas heparin lacking 6-O-sulfate groups was as active as unaltered heparin.

135 To elicit the effect, the presence of sulfate groups was necessary, yet not sufficient, as cer

136 to typical ECD behavior, localization of the sulfate groups was not possible.

137 ,2-a]carbazole also possessing sulfamate and sulfate groups, was isolated from two separate New Zeala

138 (ii) Sulfate groups were not detectable in the binding fracti

139 In both ionization modes, the sulfate groups were retained on the backbone, which allo

140 -ancorinolate B, which contain sulfamate and sulfate groups, were isolated from the aqueous extract o

141 an occupant electron density that best fit a sulfate group, which was present in the crystallization

142 otein contacts would occur by interaction of sulfate groups with basic amino acid residues on the sur

143 reted molecules that specifically remove 6-O-sulfate groups within the highly sulfated regions on HS.

144 e, an extracellular enzyme which removes 6-O sulfate groups without increasing 2-O sulfation.