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Puma expression is sufficient to induce cytochrome c loss and neuronal apoptosis.
These findings suggest that puromycin induces p53-dependent apoptosis via upregulation of RPL5 or RPL11 for binding with MDM2, and so can be used more effectively in p53 wild-type cancers by combination with RITA or doxorubicin.
Therefore, we believed that capsaicin could induce apoptosis in U251 cells, and the inhibition of autophagy could contribute to apoptosis.
Taken together, our results suggest that melatonin potentiates puromycin‐induced apoptosis with caspase‐3 and AMPK activation in HL‐60 cells, and thus, melatonin treatment can be effectively applied to leukemia treatment as a potential sensitizer for chemotherapeutic agents.
The effect of puromycin appears to be mediated by inhibition of opsonin formation rather than a puromycin-induced macrophage defect in phagocytosis.
These results suggest, that reduction of puromycin-induced apoptosis by IGF-1 occurs simultaneously with increased protein synthesis, in contrast to emetine and cycloheximide.
This report describes a bacteriocin that has the capacity to induce apoptosis in human cell lines.
Preliminary flow cytometry data suggests that compounds mentioned above induce apoptosis on these cells.
Control experiments including cycloheximide further suggested that the induction of apoptosis by puromycin was not attributable to inhibition of protein synthesis.

Related Questions

What is the molar concentration of puromycin used for assessing protein synthesis?4 answersThe molar concentration of puromycin used for assessing protein synthesis varies across the studies. In one study, the concentration of puromycin used was 49 μg/ml. Another study used concentrations of puromycin ranging from 0.1-0.5 microgram/ml. In a different study, the concentration of puromycin used was 1 μM. Additionally, the IC50 value for puromycin in inhibiting protein synthesis was reported to be 1600 ± 1200 nmol/L in HepG2 cells. Therefore, the molar concentration of puromycin used for assessing protein synthesis can vary depending on the specific experimental conditions and cell types used in each study.
Does jervinone induce apoptosis of cancer cells?4 answersJervinone does not induce apoptosis of cancer cells according to the abstracts provided. Resveratrol has been shown to induce apoptosis in pancreatic cancer cells. D limonene has been found to induce apoptosis in gastric cancer cells. Knockdown of cyclin E1 has been shown to induce apoptosis in adenocarcinoma, breast, and glioblastoma cell lines. However, there is no mention of jervinone in any of the abstracts provided.
Can phosphorylation inhibit apoptosis induction?3 answersPhosphorylation can both inhibit and induce apoptosis depending on the context. In the case of nucleolin, phosphorylation at specific sites (Thr-76 and 84) was found to be involved in protecting against myocardial ischemia/reperfusion (I/R) injury. On the other hand, hexokinase-dependent retrotranslocation of truncated BID was shown to be a selective protective mechanism against death receptor-induced apoptosis on the mitochondria. Ponicidin was found to induce apoptosis in leukemia cells by downregulating survivin and Bcl-2 expressions. Additionally, oTR was shown to induce apoptosis in SMMC-7721 cells through the activation of intrinsic mitochondria-mediated pathways. These findings suggest that phosphorylation can have both pro-apoptotic and anti-apoptotic effects depending on the specific protein and cellular context.
Can liposomes induce cell death?5 answersLiposomes have been shown to induce cell death. Liposomes loaded with photosensitizers or shikonin have demonstrated the ability to induce immunogenic cell death (ICD), which can convert tumor cells into in situ vaccines and enhance antitumor immune responses. Liposomes co-loaded with shikonin and anthracyclines have been found to induce synergistic ICD effects and cytotoxicity to tumor cells. Liposomes loaded with doxorubicin (DOX) have been developed to target tumor tissues and enhance the antitumor effect. Liposomes containing phospholipase C-related catalytically inactive protein (PRIP) have been shown to enhance cisplatin-induced apoptotic cell death in cisplatin-resistant breast cancer cells. Liposomes loaded with the cytoskeleton drug Taxotere have demonstrated a higher level of cellular inhibition and apoptosis in cells.
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