Regulation of c-jun gene expression in HL-60 leukemia cells by 1-beta-D-arabinofuranosylcytosine. Potential involvement of a protein kinase C dependent mechanism.
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Summary
The present studies in HL-60 myeloid leukemia cells indicate that the cellular response to ara-C includes the activation of protein kinase C and that aRA-C potentially induces c-jun transcription by a protein Kinase C dependent signaling mechanism.
- Type
- article
- Published
- 1991-08-13
- Cited by
- 56
- References
- 46
- OpenAlex
- https://openalex.org/W2029014224
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:28669234
Keywords
Chemistry, Gene, c-jun, BETA (programming language), Mechanism (biology)
References
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- Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.
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- Staurosporine, a potent inhibitor of phospholipid/Ca++dependent protein kinase.
- Nerve growth factor induces the proto-oncogene c-jun in PC12 cells.
- Kinetics of appearance of differentiation-associated characteristics in ML-1, a line of human myeloblastic leukemia cells, after treatment with 12-O-tetradecanoylphorbol-13-acetate, dimethyl sulfoxide or 1-beta-D-arabinofuranosylcytosine.
- DNA strand breaks caused by inhibitors of DNA synthesis: 1-beta-D-arabinofuranosylcytosine and aphidicolin.
- Enhanced jun gene expression is an early genomic response to transforming growth factor beta stimulation
- Effects of 1-beta-D-arabinofuranosylcytosine on proto-oncogene expression in human U-937 cells.
- Vasodilatory action of HA1004 [N-(2-guanidinoethyl)-5-isoquinolinesulfonamide], a novel calcium antagonist with no effect on cardiac function.
- Deoxycytidine is salvaged not only into DNA but also into phospholipid precursors. II. Ara-C does not inhibit the later process in lymphoid cells.
- Transcriptional regulation by the AP-1 family of enhancer-binding proteins: a nuclear target for signal transduction.
- Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor.
- Induction of protooncogene c-jun by serum growth factors.
- New views of the biochemistry of eucaryotic DNA replication revealed by aphidicolin, an unusual inhibitor of DNA polymerase α
- Isoquinolinesulfonamides, novel and potent inhibitors of cyclic nucleotide dependent protein kinase and protein kinase C.
- Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblasts
- A synthetic peptide substrate for selective assay of protein kinase C.
- The molecular heterogeneity of protein kinase C and its implications for cellular regulation
- Human proto-oncogene c-jun encodes a DNA binding protein with structural and functional properties of transcription factor AP-1.
Cited by
- Modulation of protein kinase C in antitumor treatment.
- Granulocyte-macrophage colony-stimulating factor/interleukin-3 fusion protein (pIXY 321) enhances high-dose Ara-C-induced programmed cell death or apoptosis in human myeloid leukemia cells.
- Ara-C: cellular and molecular pharmacology.
- Induction of nuclear factor kappa B after low-dose ionizing radiation involves a reactive oxygen intermediate signaling pathway.
- Implication of radical oxygen species in ceramide generation, c-Jun N-terminal kinase activation and apoptosis induced by daunorubicin.
- Activation of deoxycytidine kinase by inhibition of DNA synthesis in human lymphocytes.
- Effects of bryostatin 1 and other pharmacological activators of protein kinase C on 1-[beta-D-arabinofuranosyl]cytosine-induced apoptosis in HL-60 human promyelocytic leukemia cells.
- Enhancement of X-ray toxicity in squamous cell carcinoma cell lines by DNA polymerase inhibitors.
- Radiosensitization of HL-60 human leukaemia cells by bryostatin-1 in the absence of increased DNA fragmentation or apoptotic cell death.
- Coinduction of c-jun gene expression and internucleosomal DNA fragmentation by ionizing radiation.
- Effect of hemopoietic growth factors G-CSF and pIXY 321 on the activity of high dose Ara-C in human myeloid leukemia cells.
- Enzymatic rationale and preclinical support for a potent protein kinase C beta inhibitor in cancer therapy.
- Deoxycytidine kinase is phosphorylated in vitro by protein kinase C alpha.
- Comparison of idarubicin and daunorubicin regarding intracellular uptake, induction of apoptosis, and resistance.
- Intrinsic Cytotoxicity and Chemomodulatory Actions of Novel Phenethylisothiocyanate Sphingoid Base Derivatives in HL-60 Human Promyelocytic Leukemia Cells
- Involvement of reactive oxygen intermediates in the induction of c-jun gene transcription by ionizing radiation.
- Inhibition of c-Abl with STI571 attenuates stress-activated protein kinase activation and apoptosis in the cellular response to 1-beta-D-arabinofuranosylcytosine.
- Gemcitabine induces programmed cell death and activates protein kinase C in BG-1 human ovarian cancer cells
- Characteristics of the peroxisome proliferator activated receptor γ (PPARγ) ligand induced apoptosis in colon cancer cells
- The potential of protein kinase C as a target for anticancer treatment.
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