ライフサイエンスコーパス: GLUT5

1 ntroduction of four amino acids derived from GLUT5.

2 modulate the fructose transport activity of GLUT5.

3 nal part of GLUT7 and the C-terminal part of GLUT5.

4 nd inhibitor discrimination involves H387 of GLUT5.

5 rters SGLT1, GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5.

6 int in the design of specific inhibitors for GLUT5.

7 t is a tryptophan in GLUT1 but an alanine in GLUT5.

8 ral inhibitors, none have been described for GLUT5.

9 m Phytolacca americana) that inhibited human GLUT5.

10 al arginase2 (a known GR-regulated gene) and GLUT5.

11 one from allowing luminal fructose to induce GLUT5.

12 ng a similar behavior of GLUT9 compared with GLUT5.

13 ructose and express the fructose transporter GLUT5.

14 se transporter, which has been designated as GLUT5.

15 pposite was found for GLUT5 mRNA expression (GLUT5 1:6).

16 facilitative glucose transporters GLUT2 and GLUT5-12 transported DHA.

17 For rat Glut5, a change of glutamine to glutamic acid at codon 1

18 GLUT5, a fructose-transporting member of the facilitativ

19 ompanied by marked increases in brush border GLUT5 abundance, and was blocked by RU486.

20 otein has sequence identity of 44 and 38% to Glut5 and Glut1, respectively.

21 The role of the fructose transporters GLUT5 and GLUT2 in causing, contributing to or exacerbat

22 Using chimeric proteins of GLUT5 and GLUT7, here we identified amino acid residues

23 id not inhibit intestinal sugar transporters GLUT5 and SGLT1 that were injected and expressed in Xeno

24 o other major intestinal sugar transporters, GLUT5 and SGLT1, were unaffected by flavonoids.

25 lial cells and resident glia, such as CD163, Glut5, and ISG15.

26 GLUT2, GLUT5, and SGLT1 did not transport DHA and none of the i

27 d potent inhibitor of fructose transport via GLUT5, and the first chemical probe for this transporter

28 GLUT5- and GLUT2-mediated fructose effects on intestinal

29 lectivity of XylE is compared with GLUT1 and GLUT5, as well as a XylE mutant that transports D-glucos

30 hat it did not prevent fructose-induction of GLUT5, but instead prevented dexamethasone-induced synth

31 In neonatal rats, GLUT5 can be induced only by luminal fructose and only a

32 Finally, we generated a GLUT7-GLUT5 chimera consisting of the N-terminal part of GLUT7

33 Further, Glut5-deficient mice display normal OHC morphology and m

34 nisms underlying dexamethasone modulation of GLUT5 development, we first identified the receptor medi

35 tients with upregulated transcription of the GLUT5-encoding gene SLC2A5 or increased fructose utiliza

36 ddition, sequence analysis of each of the 12 GLUT5 exons was performed in the index case and confirme

37 mors, and muscle and correlated to GLUT1 and GLUT5 expression levels.

38 GLUT5 expression seems extremely low in neonatal intesti

39 c metabolite glyceraldehyde did not increase GLUT5 expression.

40 nzodioxol-5-amine (MSNBA) as an inhibitor of GLUT5 fructose transport in proteoliposomes.

41 Global expression of the GLUT5 fructose transporter and high levels of ketohexoki

42 cer cell line, MSNBA competitively inhibited GLUT5 fructose uptake with a KI of 3.2 +/- 0.4 muM.

43 To test this hypothesis, we screened the GLUT5 gene for mutations in a group of eight patients wi

44 st that IFM might be due to mutations in the GLUT5 gene.

45 nce and activity of the fructose transporter GLUT5 (glucose transporter 5) increased with fructose pe

46 rating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect.

47 r RNA, mRNA, protein, and activity levels of GLUT5 in adult wild-type mice consuming chow.

48 Fructose could not up-regulate GLUT5 in GLUT5-KO, KHK-KO, and intestinal epithelial cel

49 gulating the intestinal fructose transporter GLUT5 in vivo.

50 We show that functional expression of GLUT5 in yeast requires mutations at specific positions

51 t for high-throughput screening of potential GLUT5 inhibitors and activators, while the latter enable

52 etes, metabolic syndrome and cancer, but few GLUT5 inhibitors are known.

53 transporter and are inhibited by established GLUT5 inhibitors N-[4-(methylsulfonyl)-2-nitrophenyl]-1,

54 Human GLUT5 is a fructose-specific transporter in the glucose

55 We conclude that Glut5 is essential for the absorption of fructose in the

56 Immunolocalization studies revealed that GLUT5 is highly expressed in vivo in human breast cancer

57 We conclude that Glut5 is not required for OHC motility or cochlear ampli

58 GLUT5 is the primary transporter responsible for facilit

59 show that, in contrast to previous reports, Glut5 is undetectable, and possibly absent, in OHCs harv

60 Glucose transporter 5 (Glut5) is a high-affinity fructose transporter.

61 lucose transporter (GLUT) protein, member 5 (GLUT5) is the primary fructose transporter and that fruc

62 GLUT5-knockout (KO) mice exhibited no facilitative fruct

63 Fructose could not up-regulate GLUT5 in GLUT5-KO, KHK-KO, and intestinal epithelial cell-specifi

64 ause problems in adults unable to upregulate GLUT5 levels to match fructose concentrations in the die

65 To identify and characterize potential GLUT5 ligands, we developed a whole-cell system based on

66 ailed kinetic characterization of identified GLUT5 ligands.

67 Finally, GLUT5 may play a role in the atypical growth of certain

68 were unaffected in LEPR-B-KO jejunum, while GLUT5-mediated fructose transport and PepT1-mediated pep

69 he substrate-binding specificity by shifting Glut5-mediated transport from fructose to glucose.

70 transporter and that fructose absorption via GLUT5, metabolism via ketohexokinase (KHK), as well as G

71 However, whereas Glut5(+/+) mice showed enhanced salt absorption in their

72 h fructose (60% fructose) diet for 14 weeks, Glut5(-/-) mice did not display fructose-stimulated salt

73 n contrast to the malabsorption of fructose, Glut5(-/-) mice did not exhibit an absorption defect whe

74 Examination of the intestinal tract of Glut5(-/-) mice fed a high fructose diet revealed massiv

75 When fed a control (60% starch) diet, Glut5(-/-) mice had normal blood pressure and displayed

76 ened a library of 6 million chemicals onto a GLUT5 model and identified N-[4-(methylsulfonyl)-2-nitro

77 sue (GLUT1 50:1), the opposite was found for GLUT5 mRNA expression (GLUT5 1:6).

78 In EMT6 tumors, GLUT5 mRNA expression was 20,000-fold lower compared wit

79 F, and 1-[(18)F]FDAM does not correlate with GLUT5 mRNA levels but is linked to GLUT5 protein levels.

80 GLUT5 protein levels were higher in tumor versus muscle

81 late with GLUT5 mRNA levels but is linked to GLUT5 protein levels.

82 oes not result from the expression of mutant GLUT5 protein.

83 of an intermediate required by fructose for GLUT5 regulation.

84 ose-specific facilitative hexose transporter GLUT5 represents an alternative biomarker for PET imagin

85 is transmembrane conductance regulator), and GLUT5 required an interaction cascade of Rab11, Myo5B, S

86 Deletion of Glut5 results in a serious nutrient-absorptive defect an

87 We divided the human GLUT5 sequence into 26 fragments and then replaced each

88 Here we demonstrate that Glut5 (Slc2a5) deletion reduced fructose absorption by a

89 is mainly mediated by glucose transporter 5 (GLUT5/SLC2A5).

90 tional properties and tissue distribution of GLUT5 suggest that IFM might be due to mutations in the

91 7, here we identified amino acid residues of GLUT5 that define its substrate specificity.

92 MSNBA inhibition was specific to GLUT5; this inhibitor did not affect the fructose transp

93 abolism via ketohexokinase (KHK), as well as GLUT5 trafficking to the apical membrane via the Ras-rel

94 es fructose uptake and metabolism and normal GLUT5 trafficking to the apical membrane.

95 train deficient in fructose uptake, in which GLUT5 transport activity is associated with cell growth

96 transporters GLUT1 (transports glucose) and GLUT5 (transports fructose), in addition to their functi

97 Levels of GLUT5 were >100-fold that of candidate apical fructose t

98 ion with an upregulated fructose transporter GLUT5, which compensates for glucose deficiency.