STIMULATION OF GLUCOSE TRANSPORTER (GLUT1) MESSENGER-RNA AND PROTEIN EXPRESSION BY INHIBITORS OF GLYCOSYLATION
- Author(s)
- MAHER, F; Harrison, LC;
- Details
- Publication Year 1991-05-02,Volume 1089,Issue #1,Page 27-32
- Journal Title
- BIOCHIMICA ET BIOPHYSICA ACTA
- Publication Type
- Journal Article
- Abstract
- Glucose deprivation increases the steady-state levels of mRNA for the rat brain/HepG2-type glucose transporter (GLUT1) in L6 myocytes. Glucose deprivation also inhibits N-linked glycosylation. We therefore investigated a possible relationship between inhibition of glycosylation and GLUT1 expression in cultured L6 myocytes by determining the effects on GLUT1 expression of known inhibitors of glycosylation, namely tunicamycin, 2-deoxyglucose and glucosamine. All conditions prevented incorporation of [H-3]mannose into TCA-precipitable myocyte protein and resulted in a 2- to 5-fold increase in the level of GLUT1 mRNA detected on Northern blots. Glucose deprivation and tunicamycin treatment caused an approx. 2-fold increase in GLUT1 mRNA half-life. GLUT1 protein, detected on immunoblots, accumulated 10- to 20-fold in response to all glycosylation inhibitors, with apparent molecular masses of 40 kDa after glucose deprivation, 42 kDa after 2-deoxyglucose and 38 kDa after glucosamine or tunicamycin treatments, compared to 45-50 kDa in glucose-fed cells. However, glucose deprivation was the only condition in which the rate of 2-deoxy-[H-3]glucose uptake increased (3- to 5-fold). These results demonstrate a direct correlation between inhibition of glycosylation and the induction of GLUT1 mRNA and protein expression and suggest that the stability of GLUT1 mRNA is controlled by a signal associated with glycosylation.
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- CHICKEN-EMBRYO FIBROBLASTS; DEPENDENT REGULATION; HEXOSE TRANSPORTER; SKELETAL-MUSCLE; GENE-EXPRESSION; L6 MYOCYTES; CELLS; BIOSYNTHESIS; STARVATION; INSULIN
- Publisher's Version
- https://doi.org/10.1016/0167-4781(91)90080-6
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1991-05-02 12:00:00