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Our study showed that the additional deletion of Fa2h (show FA2H Proteins) does not obviously affect the phenotype of Cgt-/- mice. This suggests that HFA-GlcCer and HFA-sphingomyelin do not functionally compensate the loss of HFA-GalCer in Cgt-/- mice.
Ugcg (show UGCG Proteins) and Ugt8a deficient oligodendroglial did not exhibit any phenotypic or myelin structural abnormalities; abundant and structurally intact myelin can form in their absence
This study provides new insights into the changes that occur in the composition/distribution of myelin proteins in mice lacking ceramide galactosyltransferase.
Our results indicate that loss of CGT in oligodendrocytes is exclusively responsible for the myelin structural deficits, demyelination, and behavioral abnormalities in CGT-deficient mice.
An increase in the immunolabelling of ceramide was observed in cells where UDP glycosyltransferase 8 (UGT8) was down-regulated as opposed to cells where UGT8 was either not regulated or was up-regulated.
Data indicate that ceramide galactosyltransferase (show GGTA1 Proteins) (UGT8), although enhanced in non-small cell lung carcinoma (NSCLC) tissues, does not meet the criteria of a lung tumor marker.
Our study suggests that CGT expression is controlled by balanced expression of the negative modulator OLIG2 (show OLIG2 Proteins) and positive regulator Nkx2.2 (show Nkx2-2 Proteins), providing new insights into how expression of GalCer is tightly regulated in cell-type- and stage-specific manners.
A new role was identified for UGT8 as a modulator of bile acid homeostasis.
High expression of UGT8 accompanied by accumulation of GalCer in MDA-MB-231 cells is associated with a much higher proliferative index and a lower number of apoptotic cells in comparison to the MDA/LUC-shUGT8 cells.
Comprehensive genomic analyses associate UGT8 variants with musical ability in a Mongolian population.
UGT8 is a significant index of tumour aggressiveness and is seen in lung metastases of breast cancer.
Single-nucleotide polymorphisms (SNPs) were found in UGT8 gene
We postulate that molecular link between defective GALT (show GALT Proteins) enzyme, which result in classic galactosemia and the cerebroside galactosyl transferase, responsible for galactosylation of cerebrosides, is dependent on concentrations of UDP-galactose (show B4GALT1 Proteins).
The protein encoded by this gene belongs to the UDP-glycosyltransferase family. It catalyzes the transfer of galactose to ceramide, a key enzymatic step in the biosynthesis of galactocerebrosides, which are abundant sphingolipids of the myelin membrane of the central and peripheral nervous systems. Alternatively spliced transcript variants have been found for this gene.
UDP glycosyltransferase 8 (UDP-galactose ceramide galactosyltransferase)
, UDP glycosyltransferase 8
, 2-hydroxyacylsphingosine 1-beta-galactosyltransferase-like
, 2-hydroxyacylsphingosine 1-beta-galactosyltransferase
, UDP-galactose-ceramide galactosyltransferase 8A
, UDP-glucuronosyltransferase 8
, ceramide UDP-galactosyltransferase
, cerebroside synthase
, UDP-galactose ceramide galactosyltransferase
, UDP-galactose-ceramide galactosyltransferase
, uridine diphosphate glycosyltransferase 8
, UDP-galactose-ceramide galactosyltransferase 8
, UDP galactosyltransferase 8
, UDP galactosyltransferase 8A