|1.||Moriwaki, Kenta: 2 articles (01/2013 - 12/2007)|
|2.||Miyoshi, Eiji: 2 articles (01/2013 - 12/2007)|
|3.||Yakubenia, Sviatlana: 2 articles (08/2008 - 04/2007)|
|4.||Sperandio, Markus: 2 articles (08/2008 - 04/2007)|
|5.||Hellbusch, Christina C: 2 articles (08/2008 - 04/2007)|
|6.||Körner, Christian: 2 articles (08/2008 - 04/2007)|
|7.||Frommhold, David: 2 articles (08/2008 - 04/2007)|
|8.||Wild, Martin K: 2 articles (08/2008 - 04/2007)|
|9.||Yvon, Eric: 1 article (05/2015)|
|10.||Jones, Roy B: 1 article (05/2015)|
02/01/1978 - "The level of a GDP-fucose: galactoside fucosyltransferase (EC 18.104.22.168) was found elevated in nonresponding patients and was correlated with estimated tumor burden. "
08/01/1988 - "GDP-fucose:N-acetylglucosaminide alpha(1----3)-L-fucosyltransferase activity was measured in sera of patients with various cancers using a synthetic substrate, N-acetyl-2'-O-methyllactosamine, as an acceptor. "
04/01/1988 - "GDP-fucose: N-acetyl-glucosaminide alpha(1----4)-L-fucosyltransferase was demonstrated to be present in salivas from both group I and group II. These results suggest that a cancer-associated alteration of Lewis blood-group antigen expression occurs in cancer patients."
07/01/2006 - "We studied the mRNA expression levels of GDP-L-fucose-synthesizing enzymes, GDP-fucose transporter and fucosyltransferase VII by quantitative real-time PCR in mouse endothelial cells, macrophages and lymphoid tumor cells. "
12/01/1994 - "UDP-GlcNAc: Gal beta 1-3GalNAc beta 6-N-acetylglucosaminyltransferase was also decreased in cancer concomitant with a loss of the ability to synthesize the I antigen and core 4, GlcNAc beta 1-6(GlcNAc beta 1-3) GalNAc-, CMP-sialic acid: Gal beta 1-3GalNAc-R alpha 3-sialyltransferase and GDP-fucose: Gal beta-R alpha 2-fucosyltransferase, synthesizing the blood group H determinant, were found to be 4- and 3- to 8-fold increased, respectively, in cancer compared to normal tissue. "
|2.||Hepatocellular Carcinoma (Hepatoma)
12/01/2007 - "A high expression of GDP-fucose transporter in hepatocellular carcinoma is a key factor for increases in fucosylation."
07/15/1998 - "Cloning and expression of the catalytic domain from rat hepatoma H35 cell GDP-fucose:GM1 alpha 1-->2fucosyltransferase, an enzyme which is activated during early stages of chemical carcinogenesis in rat liver."
05/01/1987 - "The chemical carcinogen-induced enzyme, GDP-fucose: GM1 alpha 1----2 fucosyltransferase in rat liver and hepatoma: modulation by and association with phospholipids."
05/01/1977 - "The following three parameters were studied in Morris hepatomas of different growth rates: (a) the specific activity of guanosine dephosphate (GDP)-fucose:glycoprotein fucosyltransferase and cytidine monophosphate (CMP)-N-acetylneuraminic acid:glycoprotein sialyltransferase, (B) the content of GDP-fucosee and CMP-N-acetylneuraminic acid, and (c) the activity of alpha-L-fucosidase and neuraminidase. "
|3.||Congenital Disorders of Glycosylation
05/01/2001 - "Complementation cloning identifies CDG-IIc, a new type of congenital disorders of glycosylation, as a GDP-fucose transporter deficiency."
09/10/1999 - "We propose that this new form of carbohydrate-deficient glycoprotein syndrome is caused by impaired import of GDP-fucose into the Golgi."
09/10/1999 - "A new type of carbohydrate-deficient glycoprotein syndrome due to a decreased import of GDP-fucose into the golgi."
02/01/1998 - "In fibroblasts from five patients with carbohydrate-deficient glycoprotein syndrome type 1, the incorporation of [2-3H] mannose into mannose phosphates, GDP-mannose, GDP-fucose, dolichol-P-mannose, lipid-linked oligosaccharides, and glycoprotein fraction was determined. "
|4.||Congenital, Hereditary, and Neonatal Diseases and Abnormalities (Congenital Disorders)
02/01/2004 - "Leukocyte adhesion deficiency type II (LAD II) or the congenital disorder of glycosylation type IIc (CDG IIc) are the sole human congenital disorders known to date that are caused by a defect of GDP-fucose transport. "
08/15/2008 - "Leukocyte adhesion deficiency II (LAD II), also known as congenital disorder of glycosylation IIc (CDG-IIc), is a human disease in which a defective GDP-fucose transporter (SLC35C1) causes developmental defects and an immunodeficiency that is based on the lack of fucosylated selectin ligands. "
04/06/2007 - "Golgi GDP-fucose transporter-deficient mice mimic congenital disorder of glycosylation IIc/leukocyte adhesion deficiency II."
04/06/2007 - "The importance of fucosylation has recently been underlined by identification of the monogenetic inherited human disease "congenital disorder of glycosylation IIc," also termed "leukocyte adhesion deficiency II." Due to defective Golgi GDP-fucose transporter (SLC35C1) activity, patients show a hypofucosylation of glycoproteins and present clinically with mental and growth retardation, persistent leukocytosis, and severe infections. "
|5.||Small Cell Lung Carcinoma (Small Cell Lung Cancer)
08/01/1992 - "Presence of an essential lysine residue in a GDP-fucose protected site of the alpha 1----3fucosyltransferase from human small cell lung carcinoma NCl-H69 cells."
08/05/1990 - "Photoaffinity labeling of GDP-fucose:nLcOse4Cer alpha 1----3-fucosyltransferase from human small cell lung carcinoma NCI-H69 cells with the GDP-fucose analog GDP-hexanolaminyl-4-azidosalicylic acid."
|1.||Guanosine Diphosphate (GDP)
|3.||N-Acetylneuraminic Acid (Sialic Acid)
|4.||Uridine Diphosphate (UDP)
|6.||Messenger RNA (mRNA)
|1.||Transplantation (Transplant Recipients)