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Glucose transporter type 10 - lacking in arterial tortuosity syndrome - facilitates dehydroascorbic acid transport

Csilla E Németh, Paola Marcolongo, Alessandra Gamberucci, Rosella Fulceri, Angiolo Benedetti, Nicoletta Zoppi, Marco Ritelli, Nicola Chiarelli, Marina Colombi, Andy Willaert UGent, et al. (2016) FEBS LETTERS. 590(11). p.1630-1640
abstract
Loss-of-function mutations in the gene encoding GLUT10 are responsible for arterial tortuosity syndrome (ATS), a rare connective tissue disorder. In this study GLUT10-mediated dehydroascorbic acid (DAA) transport was investigated, supposing its involvement in the pathomechanism. GLUT10 protein produced by in vitro translation and incorporated into liposomes efficiently transported DAA. Silencing of GLUT10 decreased DAA transport in immortalized human fibroblasts whose plasma membrane was selectively permeabilized. Similarly, the transport of DAA through endomembranes was markedly reduced in fibroblasts from ATS patients. Re-expression of GLUT10 in patients' fibroblasts restored DAA transport activity. The present results demonstrate that GLUT10 is a DAA transporter and DAA transport is diminished in the endomembranes of fibroblasts from ATS patients.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
arterial tortuosity syndrome, ascorbate, VITAMIN-C, ASCORBATE, MUTATIONS, SYSTEM, LIVER MICROSOMAL VESICLES, ENDOPLASMIC-RETICULUM, MEMBRANE TRANSPORTERS, OXIDATIVE STRESS, SLC2A10 GLUT10, CANDIDATE GENE, GLUT10, dehydroascorbic acid, endomembranes, Fe2+/2-oxoglutarate-dependent dehydrogenases
journal title
FEBS LETTERS
FEBS Lett.
volume
590
issue
11
pages
1630 - 1640
Web of Science type
Article
Web of Science id
000377795000008
JCR category
BIOPHYSICS
JCR impact factor
3.623 (2016)
JCR rank
18/72 (2016)
JCR quartile
1 (2016)
ISSN
0014-5793
DOI
10.1002/1873-3468.12204
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
8051285
handle
http://hdl.handle.net/1854/LU-8051285
date created
2016-08-19 11:35:25
date last changed
2016-12-19 15:42:15
@article{8051285,
  abstract     = {Loss-of-function mutations in the gene encoding GLUT10 are responsible for arterial tortuosity syndrome (ATS), a rare connective tissue disorder. In this study GLUT10-mediated dehydroascorbic acid (DAA) transport was investigated, supposing its involvement in the pathomechanism. GLUT10 protein produced by in vitro translation and incorporated into liposomes efficiently transported DAA. Silencing of GLUT10 decreased DAA transport in immortalized human fibroblasts whose plasma membrane was selectively permeabilized. Similarly, the transport of DAA through endomembranes was markedly reduced in fibroblasts from ATS patients. Re-expression of GLUT10 in patients' fibroblasts restored DAA transport activity. The present results demonstrate that GLUT10 is a DAA transporter and DAA transport is diminished in the endomembranes of fibroblasts from ATS patients.},
  author       = {N{\'e}meth, Csilla E and Marcolongo, Paola and Gamberucci, Alessandra and Fulceri, Rosella and Benedetti, Angiolo and Zoppi, Nicoletta and Ritelli, Marco and Chiarelli, Nicola and Colombi, Marina and Willaert, Andy and Callewaert, Bert and Coucke, Paul and Gr{\'o}f, P{\'a}l and Nagy, Szilvia K and M{\'e}sz{\'a}ros, Tam{\'a}s and B{\'a}nhegyi, G{\'a}bor and Margittai, {\'E}va},
  issn         = {0014-5793},
  journal      = {FEBS LETTERS},
  keyword      = {arterial tortuosity syndrome,ascorbate,VITAMIN-C,ASCORBATE,MUTATIONS,SYSTEM,LIVER MICROSOMAL VESICLES,ENDOPLASMIC-RETICULUM,MEMBRANE TRANSPORTERS,OXIDATIVE STRESS,SLC2A10 GLUT10,CANDIDATE GENE,GLUT10,dehydroascorbic acid,endomembranes,Fe2+/2-oxoglutarate-dependent dehydrogenases},
  language     = {eng},
  number       = {11},
  pages        = {1630--1640},
  title        = {Glucose transporter type 10 - lacking in arterial tortuosity syndrome - facilitates dehydroascorbic acid transport},
  url          = {http://dx.doi.org/10.1002/1873-3468.12204},
  volume       = {590},
  year         = {2016},
}

Chicago
Németh, Csilla E, Paola Marcolongo, Alessandra Gamberucci, Rosella Fulceri, Angiolo Benedetti, Nicoletta Zoppi, Marco Ritelli, et al. 2016. “Glucose Transporter Type 10 - Lacking in Arterial Tortuosity Syndrome - Facilitates Dehydroascorbic Acid Transport.” Febs Letters 590 (11): 1630–1640.
APA
Németh, C. E., Marcolongo, P., Gamberucci, A., Fulceri, R., Benedetti, A., Zoppi, N., Ritelli, M., et al. (2016). Glucose transporter type 10 - lacking in arterial tortuosity syndrome - facilitates dehydroascorbic acid transport. FEBS LETTERS, 590(11), 1630–1640.
Vancouver
1.
Németh CE, Marcolongo P, Gamberucci A, Fulceri R, Benedetti A, Zoppi N, et al. Glucose transporter type 10 - lacking in arterial tortuosity syndrome - facilitates dehydroascorbic acid transport. FEBS LETTERS. 2016;590(11):1630–40.
MLA
Németh, Csilla E, Paola Marcolongo, Alessandra Gamberucci, et al. “Glucose Transporter Type 10 - Lacking in Arterial Tortuosity Syndrome - Facilitates Dehydroascorbic Acid Transport.” FEBS LETTERS 590.11 (2016): 1630–1640. Print.