NCBI . NLM . NIH . GOV {
}
We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC5915869/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC5915869/. The analysis below is for the second page.
Title[redir]:
ΔNp63 Inhibits Oxidative Stress-Induced Cell Death Including Ferroptosis and Cooperates with the BCL-2 Family to Promote Clonogenic Survival - PMC
Description:
The BCL-2 family proteins are central regulators of apoptosis. However, cells deficient for BAX and BAK or overexpressing BCL-2 still succumb to oxidative stress upon DNA damage or matrix detachment. Here, we show that ΔNp63α overexpression protects ...
Title[redir]:
ΔNp63 Inhibits Oxidative Stress-Induced Cell Death Including Ferroptosis and Cooperates with the BCL-2 Family to Promote Clonogenic Survival - PMC
Description:
The BCL-2 family proteins are central regulators of apoptosis. However, cells deficient for BAX and BAK or overexpressing BCL-2 still succumb to oxidative stress upon DNA damage or matrix detachment. Here, we show that ΔNp63α overexpression protects ...
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🌠 Phenomenal Traffic: 5M - 10M visitors per month
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Keywords {🔍}
δnpα, cell, cells, doi, death, oxidative, figure, glutathione, stress, pubmed, google, scholar, mefs, bcl, dna, ros, pmc, cancer, transduced, genes, expression, article, data, lung, survival, free, retrovirus, overexpression, quantified, ferroptosis, knockdown, mcfa, apoptosis, metabolism, etoposide, damage, human, baxbak, shown, gclc, svtransformed, treated, nature, staining, squamous, untreated, figures, analyzed, samples, promote,
Topics {✒️}
apoptosis-deficient bax-/-bak-/- double-knockout luciferase-transduced mda-mb-231 cells p53-/-bax-/-bak-/- triple-knockout antioxidants n-acetyl-l-cysteine bcl-xl-overexpressing p53-deficient mefs n-terminal flag-ha-tagged δnp63α antioxidant n-acetyl-l-cysteine transformed bax-/-bak-/- mefs p53-/-bax-/-bak-/- tko cells lentiviral tetracycline-inducible system long-term clonogenic survival limits long-term survival promoting long-term survival n-acetyl-l-cysteine short-term survival advantage long-term cellular wellbeing bax-/-bak-/- dko mefs beas-2b cells transduced investigate long-term survival cross-reactive band serving p53-/-bax-/-bak-/- cells pmc beta search high-resolution genomic profiles cytokine/growth factor deprivation dna damage-induced death somatic copy-number alteration promote anchorage-independent growth bax-/-bak-/- cells showed ros-induced cell death promotes anchorage-independent growth wilcoxon rank-sum test chamber slide pre-coated bak-mediated mitochondrial apoptosis etoposide-induced cell death dna damage-induced pnd sv40-transformed wt genotoxic stress-induced ros supplementary materials included detecting p53-responsive genes protecting apoptosis-defective cells poly-hema-coated plates δnp63α protected wild-type broad-spectrum ros indicator etoposide-induced ros accumulation hcc95 cell line mcf-10a cells transduced inhibit etoposide-induced death references balaban rs lentivirus-mediated knockdown constructs tp63 amplification/overexpression upregulates
Questions {❓}
- Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?
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