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Solute carrier family 35, member C1

GDP-fucose transporter, SLC35C1, FucTI
This gene encodes a GDP-fucose transporter that is found in the Golgi apparatus. Mutations in this gene result in congenital disorder of glycosylation type IIc. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Feb 2009] (from NCBI)
Top mentioned proteins: fucosyltransferase, Cho, CAN, ACID, HAD
Papers on GDP-fucose transporter
A microdeletion encompassing PHF21A in an individual with global developmental delay and craniofacial anomalies.
Kim et al., Augusta, United States. In Am J Med Genet A, Dec 2015
Using microarray, qPCR, RT-qPCR, and Western blot analyses, we refined the candidate gene region, which harbors five genes, by excluding two genes, SLC35C1 and CRY2, which resulted in a corroborating role of PHF21A in developmental delay and craniofacial anomalies.
Inactivation of GDP-fucose transporter gene (Slc35c1) in CHO cells by ZFNs, TALENs and CRISPR-Cas9 for production of fucose-free antibodies.
Song et al., Singapore, Singapore. In Biotechnol J, Nov 2015
While previous works have shown that inactivation of fucosyltransferase 8 (FUT8) results in mutants capable of producing fucose-free antibodies, we report here the use of genome editing techniques, namely ZFNs, TALENs and the CRISPR-Cas9, to inactivate the GDP-fucose transporter (SLC35C1) in CHO cells.
Fucosylation is a common glycosylation type in pancreatic cancer stem cell-like phenotypes.
Miyoshi et al., Suita, Japan. In World J Gastroenterol, May 2015
However, downregulation of cellular fucosylation by knockdown of the GDP-fucose transporter did not alter gemcitabine resistance, indicating that increased cellular fucosylation is a result of CSC-like transformation.
Negative feedback regulation of Wnt signaling via N-linked fucosylation in zebrafish.
Marlow et al., United States. In Dev Biol, 2014
To study how changes in fucosylation impact embryonic development, we up-regulated N-linked fucosylation via over-expression of a key GDP-Fucose transporter, Slc35c1, in zebrafish.
Congenital disorder of fucosylation type 2c (LADII) presenting with short stature and developmental delay with minimal adhesion defect.
Sackstein et al., In Hum Mol Genet, 2014
Leukocyte adhesion deficiency type II is a hereditary disorder of neutrophil migration caused by mutations in the guanosine diphosphate-fucose transporter gene (SLC35C1).
Decreased core-fucosylation contributes to malignancy in gastric cancer.
Gao et al., Shanghai, China. In Plos One, 2013
The recombinant plasmids of GDP-fucose transporter and α-1,6-fucosyltransferase (Fut8) were constructed and transfected into gastric cancer cell lines BGC-823 and SGC-7901.
Roles of the nucleotide sugar transporters (SLC35 family) in health and disease.
Song, Singapore, Singapore. In Mol Aspects Med, 2013
Mutations in two NST genes, SLC35A1 and SLC35C1, have been related to congenital disorder of glycosylation II (CDG II).
A 137-kb deletion within the Potocki-Shaffer syndrome interval on chromosome 11p11.2 associated with developmental delay and hypotonia.
Aylsworth et al., Chapel Hill, United States. In Am J Med Genet A, 2013
This deletion results in haploinsufficiency for all or portions of six OMIM genes: SLC35C1, CRY2, MAPK8IP1, PEX16, GYLTL1B, and PHF21A.
Transforming growth factor β signaling upregulates the expression of human GDP-fucose transporter by activating transcription factor Sp1.
Liu et al., Boston, United States. In Plos One, 2012
GDP-fucose transporter plays a crucial role in fucosylation of glycoproteins by providing activated fucose donor, GDP-fucose, for fucosyltransferases in the lumen of the Golgi apparatus.
Identification of functional elements of the GDP-fucose transporter SLC35C1 using a novel Chinese hamster ovary mutant.
Song et al., Singapore, Singapore. In Glycobiology, 2012
the conserved glycine residues at positions 180 and 277 of SLC35C1 have significant impacts on lectin binding
Hematologically important mutations: leukocyte adhesion deficiency (first update).
Roos et al., Amsterdam, Netherlands. In Blood Cells Mol Dis, 2012
In the rare LAD-II disease, the fucosylation of selectin ligands is disturbed, caused by mutations in SLC35C1, the gene that encodes a GDP-fucose transporter of the Golgi system. (Review)
Leukocyte adhesion deficiency type II: long-term follow-up and review of the literature.
Garty et al., Israel. In J Clin Immunol, 2010
Genetic analysis of the Golgi GDP-fucose transporter (GFTP) sequence yielded a point mutation resulting in Y337C amino acid transition in the tenth transmembrane domain.
Biological function of fucosylation in cancer biology.
Nakagawa et al., Suita, Japan. In J Biochem, 2008
Many kinds of fucosyltransferases, the GDP-fucose synthesis pathway and GDP-fucose transporter are involved in the regulation of fucosylation.
A high expression of GDP-fucose transporter in hepatocellular carcinoma is a key factor for increases in fucosylation.
Miyoshi et al., Suita, Japan. In Glycobiology, 2007
the upregulation of GDP-Fuc Tr plays a pivotal role in increased fucosylation in hepatocellular carcinoma
Nucleotide-sugar transporters: structure, function and roles in vivo.
Orellana et al., Santiago, Chile. In Braz J Med Biol Res, 2006
In humans, the mutation of a GDP-fucose transporter is responsible for an impaired immune response as well as retarded growth.
Leukocyte adhesion deficiency II patients with a dual defect of the GDP-fucose transporter.
Wild et al., Münster, Germany. In Blood, 2006
Leukocyte adhesion deficiency II patients display dual defect in functoin ang Golgi expression of FUCT1.
Insights into leukocyte adhesion deficiency type 2 from a novel mutation in the GDP-fucose transporter gene.
Frenette et al., New York City, United States. In Blood, 2003
In the GDP-fucose transporter a new single nucleotide deletion produced an open-reading frame shift & polypeptide truncation. Overexpression of the mutant protein in fibroblasts did not rescue fucosylation. The deletion ablated transporter activity.
Complementation cloning identifies CDG-IIc, a new type of congenital disorders of glycosylation, as a GDP-fucose transporter deficiency.
Körner et al., Göttingen, Germany. In Nat Genet, 2001
Restoration of GDP-fucose import activity in Golgi-enriched vesicles from the patient's fibroblasts verified the GDP-fucose transporter activity of this protein.
The gene defective in leukocyte adhesion deficiency II encodes a putative GDP-fucose transporter.
Vestweber et al., Bad Nauheim, Germany. In Nat Genet, 2001
Thus, we have identified the first putative GDP-fucose transporter, which has been highly conserved throughout evolution.
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