These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Regulation of the expression of galactoside-binding lectin during human monocytic differentiation.
    Author: Nangia-Makker P, Ochieng J, Christman JK, Raz A.
    Journal: Cancer Res; 1993 Oct 15; 53(20):5033-7. PubMed ID: 8402696.
    Abstract:
    The widely distributed hL-31 (CBP35, epsilon BP, mL-34, L-29, Mac-2) is a Ca(2+)-independent galactoside-binding lectin which functions as a receptor on mammalian cells for glycoproteins containing poly-N-acetyllactosamine side chains. Little is known about the regulation of its expression. The human promyelocytic leukemia cell line, HL-60, was used to determine whether expression of hL-31 (Mac-2) correlated with macrophage/monocyte differentiation. Nondifferentiated HL-60 cells and HL-60 cells grown in the presence of 1.24 microM retinoic acid expressed only trace amounts of hL-31. In contrast, both hL-31 transcripts and protein were detected at 8 h after addition of 17 nM 12-O-tetradecanoylphorbol-13-acetate and reached maximal levels at 24 h. Addition of actinomycin D along with 12-O-tetradecanoylphorbol-13-acetate blocked accumulation of hL-31 mRNA. In contrast, addition of actinomycin D to 12-O-tetradecanoylphorbol-13-acetate-treated HL-60 cells that had already accumulated high levels of hL-31 mRNA did not cause significant reduction in RNA levels until 6-8 h had elapsed. Since increased hL-31 expression was not associated with an increase in transcriptional activity of the hL-31 gene, these results suggest that hL-31 expression is regulated at the posttranscriptional level, at least in part, by stabilization of its mRNA. The results also indicate that the processes leading to increased hL-31 expression in HL-60 cells may be specific to differentiation along the monocyte/macrophage pathway.
    [Abstract] [Full Text] [Related] [New Search]