FUT2


Also found in: Dictionary, Thesaurus, Financial, Encyclopedia.
Related to FUT2: Lewis Blood Group

FUT2

A gene on chromosome 19q13.3 that encodes a Golgi membrane protein involved in synthesising an H-antigen precursor, which is required for the final step in synthesising soluble A and B antigens. FUT2 is one of two genes that encode galactoside 2-L-fucosyltransferase.
Mentioned in ?
References in periodicals archive ?
Relationship of FUT2 Gene Polymorphisms with the Clinical Pathogenic Characteristics of IBD Patients.
In CD patients, the mutant allele (T) and genotype (AT+TT) of FUT2 A385T were less prevalent in patients with ileocolonic CD than in colonic CD (41.67% versus 59.41%, P = 0.001, OR = 0.488, and 95% CI = 0.324-0.734; 63.33% versus 83.17%, P = 0.002, OR = 0.350, and 95% CI = 0.178-0.686, resp.) (Table 4).
patients by ABO blood rotavirus group and Lewis antigen strain, status ([dagger]) patient FUT2 genotype O A B Le+ Le- Le+ Le- Le+ G9P[8] 4 0 1 0 2 Se/Se 0 0 1 0 1 Se/se 4 0 0 0 1 se/se 0 0 0 0 0 G3P[8] 1 0 4 0 2 Se/Se 0 0 2 0 1 Se/se 1 0 1 0 1 se/se 0 0 0 0 0 G1P[8] 4 0 3 0 0 Se/Se 0 0 0 0 0 Se/se 4 0 2 0 0 G4P[8] 1 0 1 0 0 Se/se 0 0 1 0 0 G2P[4] 2 0 0 0 0 Se/Se 1 0 0 0 0 P[8] 0 0 1 0 0 Se/Se 0 0 1 0 0 Total 12 0 10 0 4 Se/Se 1 0 4 0 2 Se/se 9 0 4 0 2 se/se 0 0 0 0 0 Isolated No.
Sequence and expression of a candidate for the human Secretor blood group [alpha](1,2)fucosyltransferase gene (FUT2): homozygosity for an enzyme-inactivating nonsense mutation commonly correlates with the non-secretor phenotype.
Missense mutation of FUT1 and deletion of FUT2 are responsible for Indian Bombay phenotype of ABO blood group system.
To determine whether 3-D intestinal aggregates contain the FUT2 gene that converts precursor molecules to H-type antigens (21), we performed genotyping analysis on the INT-407 intestinal cells used to produce the organotypic cell culture model.
Previous studies determined that overexpression of FUT2 in natively nonexpressing or low-expressing cell types, or upon differentiation of Caco-2 cells that natively express FUT2, results in a dramatic increase in NV particle binding (5,19,32,37,38).
The coding sequence of FUT2 was sequenced completely in one nonsecretor individual and partially in two secretor-positive individuals.
PCR was used to amplify the coding sequence of FUT2. Sequencing of the PCR products was carried out using the ABI PRISM dRhodamine Terminator Cycle Sequencing Ready Reaction Kit with AmpliTaq DNA Polymerase FS (Perkin-Elmer), according to the manufacturer's protocol, and a model 377 DNA sequencer (Applied Biosystems).
Although human NoV susceptibility is highly associated with secretor status, and thus with mutations in FUT2 (4), no information is yet available on whether host genetic factors determine susceptibility to SaV.
A single nucleotide polymorphism at position 428 in the FUT2 gene was investigated by pyrosequencing (3,11).
Although NoV infections of secretors are well documented (18) and a few cases of infected nonsecretors have been reported (19,20), no virus has been identified in authentic outbreaks that is completely secretor or Lewis antigen independent, where homozygous carriers of the nonsense G428A mutation in FUT2 are at similar or higher risk for infection than are secretors.