Title : Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.

Pub. Date : 1990 Feb 25

PMID : 2105946






11 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 AP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
2 AP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
3 We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
4 Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
5 Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
6 TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
7 The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
8 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
9 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
10 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
11 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens