ライフサイエンスコーパス: GDP fucose

1 th proteins were able to salvage l-fucose to GDP-fucose.

2 to synthesize the donor for fucose addition, GDP-fucose.

3 e one to rescue designer mice unable to make GDP-Fucose.

4 residue that lies near the binding site for GDP-fucose.

5 -5'-[alpha-(32)P] triphosphate, an analog of GDP-fucose.

6 involved in the conversion of GDP-mannose to GDP-fucose.

7 nerate GDP-Arap, while synthesizing abundant GDP-fucose.

8 -1-P toward GTP, leading to the formation of GDP-fucose.

9 De novo synthesis of guanosine diphosphate (GDP)-fucose, a substrate for fucosylglycans, requires se

10 De novo synthesis of guanosine diphosphate (GDP)-fucose, a substrate for fucosylglycans, requires se

11 CB CD34(+) cells with guanosine diphosphate (GDP) fucose and exogenous alpha1-3 fucosyltransferase VI

12 charide linked to C-6 of a fucose residue in GDP-fucose and a milk fucosyltransferase.

13 Kinetic analysis indicates that GDP-fucose and xyloglucan associate with the enzyme in a

14 he Km values for factor VII EGF-1 domain and GDP-fucose are 15 and 6 microM, respectively.

15 Given that bulkier analogs like GDP-fucose are also accommodated at this site, it seems

16 fut1 (protein-O-fucosyltransferase-1) linked GDP-fucose availability to downstream Notch-Rbpj signali

17 ing pocket of SPY and competitively inhibits GDP-fucose binding.

18 l analyses predicted that SOFTI binds to the GDP-fucose-binding pocket of SPY and competitively inhib

19 for site-specific fucosylation map near the GDP-fucose-binding site.

20 Injection of GDP-fucose but not fucose into C. elegans intestinal cel

21 up designed to mimic the transition state of GDP-fucose complexed with Mn(II) in fucosyltransferase r

22 ogenous alpha1-3-fucosyltransferase FTVI and GDP-fucose created many new epitopes for anti-sLe(x) mAb

23 on produce the same biochemical phenotype of GDP-fucose deficiency.

24 This supports the hypothesis that GDP-fucose exists in multiple, distinct pools, not as a

25 These results establish a requirement for GDP-fucose for L. major viability and predict the existe

26 No significant change occurred in the Km for GDP-fucose for this protein when compared with FucT V.

27 We measured the contribution of GDP-fucose from each of these sources for glycan synthes

28 alyzes the first step in the biosynthesis of GDP-fucose from GDP-mannose.

29 ndependent transport preferentially utilized GDP-fucose from the salvage pathway over the de novo bio

30 Previous analyses showed the presence of GDP-fucose (GDP-Fuc), the precursor for all fucosylation

31 A GDP-fucose:GM1 alpha1-->2 fucosyltransferase (FucT) is i

32 one are sufficient to convert GDP mannose to GDP fucose in vitro.

33 e, UDP-N-acetylglucosamine, GDP-mannose, and GDP-fucose in Plasmodium falciparum intraerythrocytic li

34 those observed in mice unable to synthesize GDP-fucose, indicating the existence of another mechanis

35 aling distinct active-site features enabling GDP-fucose instead of UDP-GlcNAc binding.

36 lc35c1 encodes an antiporter that transports GDP-fucose into the Golgi and returns GMP to the cytopla

37 syltransferase that incorporates fucose from GDP-fucose into xyloglucan, adding it preferentially to

38 Starting from L-fucose, GDP-fucose is constructed by one bifunctional enzyme L-f

39 at are active in vitro, indicating that most GDP-fucose is formed by a de novo pathway that involves

40 To test whether GDP-fucose itself was essential for Leishmania viability

41 lbeta(1-->4)GlcNAc unit, and a corresponding GDP-fucose:N-acetylglucosaminyl alpha(1,3) fucosyltransf

42 a neutral pH optimum, and exhibited a Km for GDP-fucose of 0.34 microM, a Km for pNP-LNB of 0.6 mM, a

43 e transporter that competes with Slc35c1 for GDP-fucose, or a factor that otherwise enhances the fuco

44 ion of the transporters for CMP-sialic acid, GDP-fucose, or both unexpectedly resulted in accumulatio

45 A GDP-fucose:polypeptide fucosyltransferase was purified 5

46 ucose residues identify and select different GDP-fucose pools dependent on their heritage.

47 Thus, the GDP-fucose precursor is essential in a wide variety of o

48 These critical findings identify de novo GDP-fucose production as a novel metabolic vulnerability

49 NBs were found to be dependent upon de novo GDP-fucose production to sustain cell surface and secret

50 No change in GDP-fucose-protectable pyridoxal-P/NaBH4 inactivation wa

51 ose to epidermal growth factor-like repeats, GDP-fucose protein O-fucosyltransferase (O-FucT-1), was

52 This method exploits l-fucokinase/GDP-fucose pyrophosphorylase (FKP), a bifunctional enzym

53 bifunctional polypeptide called L-fucokinase/GDP-fucose pyrophosphorylase (FKP), which has attracted

54 L-fucokinase (FUK) and GDP-fucose pyrophosphorylase (GFPP) salvage free L-fucos

55 yo-EM) structure of SPY and its complex with GDP-fucose, revealing distinct active-site features enab

56 re deficient in conversion of GDP-mannose to GDP-fucose substantially decreased the levels of secrete

57 n the parasite is not known, the presence of GDP-fucose suggests that the metabolite may be used for

58 a lack of fucosylation consequent to loss of GDP-fucose synthesis contributes to colon carcinogenesis

59 the trypanosomatid parasite Leishmania While GDP-Fucose synthesis is essential, fucosylated glycoconj

60 encodes an enzyme in the de novo pathway for GDP-fucose synthesis, exhibit a virtually complete defic

61 ive in N-acetylglucosaminyltransferase V and GDP-fucose synthesis, respectively, demonstrating that a

62 etary fucose to supply a salvage pathway for GDP-fucose synthesis.

63 -committed and rate-limiting step of de novo GDP-fucose synthesis.

64 Escherichia coli GDP-mannose dehydratase and GDP-fucose synthetase (GFS) protein have been cloned and

65 ay enzymes GDP-mannose dehydratase (GMD) and GDP-fucose synthetase (GMER) were expressed ectopically;

66 GDP-fucose synthetase from E. coli is a novel dual funct

67 ined guanidine 5'-diphosphate-beta-l-fucose (GDP-fucose), the universal fucosyl donor, the Le(x) tris

68 nylfucose derivatives that depleted cells of GDP-fucose, the substrate used by fucosyltransferases to

69 These cells cannot synthesize GDP-fucose through the de novo pathway, and lack fucosyl

70 (FucT) catalyzes the transfer of fucose from GDP-fucose to asparagine-linked GlcNAc of the N-glycan c

71 Fucose transfer from GDP-fucose to GlcNAc residues of the sialylated polylact

72 e FUT1 catalyzes the transfer of fucose from GDP-fucose to terminal galactosyl residues on xyloglucan

73 cing of GDP-L-fucose synthetase (FX) and the GDP-fucose transmembrane transporter (SLC35C1), both piv

74 sphatidylcholine liposomes, it was active in GDP-fucose transport and was specifically photolabeled w

75 our results imply that the Golgi systems of GDP-fucose transport discriminate between substrate pool

76 by leucine in nac(1) flies, which abolishes GDP-fucose transport in vivo and in vitro.

77 A defect in GDP-fucose transport into the lumen of the Golgi apparat

78 re abrogated, at least one more mechanism of GDP-fucose transport into the secretory pathway must exi

79 ating the existence of another mechanism for GDP-fucose transport into the secretory pathway.

80 ects and embryonic lethality expected if all GDP-fucose transport were abrogated, at least one more m

81 existence of an SLC35C1-independent route of GDP-fucose transport, which remains a mystery.

82 that a conserved serine residue in the Golgi GDP-fucose transporter (GFR) is substituted by leucine i

83 genes encoding either POFUT2 or the putative GDP-fucose transporter (NST2) resulted in loss of MIC2 O

84 Here we identify GDP-fucose transporter 1 (GFT1), an Arabidopsis nucleoti

85 sely related gene Slc35c2 encodes a putative GDP-fucose transporter and promotes Notch fucosylation a

86 tions in the SLC35C1 gene encoding the Golgi GDP-fucose transporter are known to cause leukocyte adhe

87 A potential candidate for a second GDP-fucose transporter is the related gene Slc35c2.

88 he ER, suggesting that a novel, ER-localized GDP-fucose transporter may exist.

89 Inactivation of the Golgi GDP-fucose transporter Slc35c1 in mouse or human does no

90 ned results suggest that Slc35c2 is either a GDP-fucose transporter that competes with Slc35c1 for GD

91 ed and purified the rat liver Golgi membrane GDP-fucose transporter, a protein with an apparent molec

92 en that the absence of both SLC35C1, a known GDP-fucose transporter, and SLC35C2, a putative GDP-fuco

93 -fucose transporter, and SLC35C2, a putative GDP-fucose transporter, did not lead to afucosylated NOT

94 It is caused by mutations in the Golgi GDP-fucose transporter, resulting in a reduction of fuco

95 ed fucosylation via over-expression of a key GDP-Fucose transporter, Slc35c1, in zebrafish.

96 SQV-7 did not transport CMP-sialic acid, GDP-fucose, UDP-N-acetylglucosamine, UDP-glucose, or GDP

97 fragilis 9343, which converts l-fucose into GDP-fucose via a fucose-1-phosphate (Fuc-1-P) intermedia

98 Ac) and 4-fold reduction in its affinity for GDP-fucose when compared with FucT III.