Phorbol ester treatment of HL 60 leukemia cells results in increase of beta-(1 --> 4)-galactosyltransferase.
We previously showed that HL 60 leukemia cells exhibit various changes in their cellular glycans after phorbol 12-myristate 13-acetate (PMA) treatment. These changes could originate largely from changes in one or several glycosyltransferases. In this report, we show using enzymatic measures, fluorescence microscopy, immunoblotting and Northern blot that beta-(1 --> 4)-galactosyltransferase I (GalT I) activity was higher (> x 2) in PMA-treated compared with untreated HL 60 cells. Immunoblotting showed an increased intensity of the GalT I band at 49 kDa and Northern blot a weak increase of the GalT I transcript band, after PMA treatment. Moreover, Northern blot performed after actinomycin-D treatment of the cells, which inhibits transcription, suggests that the observed increase of GalT I expression could originate, in part, from increase of the stability of GalT I transcripts.
Pasqualetto
V
V
Université de Paris V-René Descartes, UFR Biomédicale des Saints-Pères, France.
Lemaire
S
S
Neel
D
D
Aubery
M
M
Berger
E G
EG
Derappe
C
C
D015152:Blotting, Northern; D005700:Galactosyltransferases / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D018922:HL-60 Cells; D006801:Humans; D015151:Immunoblotting; D008856:Microscopy, Fluorescence; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D012333:RNA, Messenger; D005700:Galactosyltransferases; C119701:beta-1,4-galactosyltransferase I; D013755:Tetradecanoylphorbol Acetate