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.
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Summary
Assessment of DNA damage by quantitative spectrofluorophotometry of small molecular weight, double-stranded DNA fragments provided a more complete characterization of the interaction between ara-C and bryostatin 1, and a direct comparison of the relative effects of brystatin 1 treatment with other pharmacological manipulations known to modulate protein kinase C activity.
- Type
- article
- Published
- 1994-03-02
- Cited by
- 87
- References
- 50
- OpenAlex
- https://openalex.org/W1967439648
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:38109722
Keywords
Bryostatin 1, DNA fragmentation, Apoptosis, Protein kinase C, Fragmentation (computing)
References
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- Apoptosis: a different type of cell death
- Internucleosomal DNA fragmentation during phorbol ester-induced monocytic differentiation and G0/G1 arrest.
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- Bryostatin, an activator of the calcium phospholipid-dependent protein kinase, blocks phorbol ester-induced differentiation of human promyelocytic leukemia cells HL-60.
- HL‐60 cells induced to differentiate towards neutrophils subsequently die via apoptosis
Cited by
- 12-O-tetradecanoylphorbol-13-acetate-induced Apoptosis Is Mediated by Tumor Necrosis Factor α in Human Monocytic U937 Cells*
- Phase I Study of Prolonged Infusion Bryostatin-1 in Patients
- Potential for protein kinase C inhibitors in cancer therapy.
- Modulation of protein kinase C in antitumor treatment.
- Multifunctional modulators of drug resistance.
- Low dose docosahexaenoic acid protects normal colonic epithelial cells from araC toxicity
- Activated calphostin C cytotoxicity is independent of p53 status and in vivo metastatic potential.
- Ceramide: a novel lipid mediator of apoptosis.
- Ara-C: cellular and molecular pharmacology.
- Inhibition of protein kinase C activator-mediated induction of p21CIP1 and p27KIP1 by deoxycytidine analogs in human leukemia cells: relationship to apoptosis and differentiation.
- Protein Kinase C Targeting in Antineoplastic Treatment Strategies
- Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cells.
- Implication of radical oxygen species in ceramide generation, c-Jun N-terminal kinase activation and apoptosis induced by daunorubicin.
- Agents that down-regulate or inhibit protein kinase C circumvent resistance to 1-beta-D-arabinofuranosylcytosine-induced apoptosis in human leukemia cells that overexpress Bcl-2.
- Effects of modulators of protein kinases on taxol-induced apoptosis of human leukemic cells possessing disparate levels of p26BCL-2 protein.
- Dysregulation of the cyclin-dependent kinase inhibitor p21WAF1/CIP1/MDA6 increases the susceptibility of human leukemia cells (U937) to 1-beta-D-arabinofuranosylcytosine-mediated mitochondrial dysfunction and apoptosis.
- Protein Kinase C: A Target for Therapy in Pancreatic Cancer
- Sensitization of human breast cancer cells to gemcitabine by the protein kinase C modulator bryostatin 1
- Phase I study of bryostatin-1 in combination with cisplatin in treating patients with metastatic or unresectable solid tumors including non small-cell lung cancer.
- Effect of bryostatin 1 on taxol-induced apoptosis and cytotoxicity in human leukemia cells (U937).
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