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We are analyzing https://www.nature.com/articles/s41417-020-0170-2.

Title:
Transcription factors in ferroptotic cell death | Cancer Gene Therapy
Description:
Ferroptosis, a form of regulated cell death, is characterized by an excessive degree of iron accumulation and lipid peroxidation. Although it was originally identified only in cells expressing a mutant RAS oncogene, ferroptosis has also been found in normal cells following treatment by small molecules (e.g., erastin and RSL3) or drugs (e.g., sulfasalazine, sorafenib, and artesunate), which target antioxidant enzyme systems, especially the amino acid antiporter system xcโˆ’ and the glutathione peroxidase GPX4. Dysfunctional ferroptosis is implicated in various physiological and pathological processes (e.g., metabolism, differentiation, and immunity). Targeting the ferroptotic network appears to a new treatment option for diseases or pathological conditions (e.g., cancer, neurodegeneration, and ischemia reperfusion injury). While the molecular machinery of ferroptosis remains largely unknown, several transcription factors (e.g., TP53, NFE2L2/NRF2, ATF3, ATF4, YAP1, TAZ, TFAP2C, SP1, HIF1A, EPAS1/HIF2A, BACH1, TFEB, JUN, HIC1, and HNF4A) play multiple roles in shaping ferroptosis sensitivity through either transcription-dependent or transcription-independent mechanisms. In this review, we summarize recent progress in understanding the transcriptional regulation underlying ferroptotic cell death, and discuss how it has provided new insights into cancer therapy.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {๐Ÿ“š}

  • Education
  • Health & Fitness
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Content Management System {๐Ÿ“}

What CMS is nature.com built with?

Custom-built

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๐Ÿš€๐ŸŒ  Tremendous Traffic: 10M - 20M visitors per month


Based on our best estimate, this website will receive around 19,927,269 visitors per month in the current month.

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Display Ads {๐ŸŽฏ}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

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Direct Advertisers (10)
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Display Ads {๐ŸŽฏ}

$251,100 per month
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Keywords {๐Ÿ”}

pubmed, google, scholar, cas, ferroptosis, cancer, cell, central, death, nature, cells, wang, biol, zhang, chen, kang, liu, tang, res, sun, article, ferroptotic, nat, gene, access, nrf, rev, yang, sci, content, zhu, biochem, glutathione, gpx, mechanisms, regulation, role, human, autophagy, commun, pathway, cookies, therapy, transcription, dai, lipid, metabolism, sensitivity, xie, stockwell,

Topics {โœ’๏ธ}

nature portfolio permissions reprints privacy policy medical research author information authors advertising cystine/glutamate antiporter xct p62-keap1-nrf2 pathway protects nature social media targeting ets1/gpx4-mediated ferroptosis glutamate-cysteine ligase inhibitors oxidative stress-induced apoptosis p53-mediated ferroptotic responses gpx4 inhibitor-induced ferroptosis genotype-selective antitumor agents ap-2gamma promotes proliferation jtc801 induces ph-dependent cell-line selectivity improves exosomal mir-499a-5p er stress-independent ferroptosis gcn2-eif2alpha-atf4 pathway glutathione-independent ferroptosis suppressor autophagy-dependent cell death cancer-acquired drug resistance atf4-chop-chac1 pathway p53-mediated tumour suppression personal data friedmann angeli jp rui kangย &ย daolin tang ferroptotic cell death 1038/s41417-019-0134-6 [epub ahead transcription-independent p53 apoptosis data protection springerlink instant access permissions glutathione peroxidase gpx4 published maps european economic area promote clonogenic survival ferroptotic network appears renal cell carcinoma xct-dependent manner induced cytotoxic effects mir-137 regulates ferroptosis regulated cell death human breast cancer nonapoptotic cell death cell death differ cell death dis

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         headline:Transcription factors in ferroptotic cell death
         description:Ferroptosis, a form of regulated cell death, is characterized by an excessive degree of iron accumulation and lipid peroxidation. Although it was originally identified only in cells expressing a mutant RAS oncogene, ferroptosis has also been found in normal cells following treatment by small molecules (e.g., erastin and RSL3) or drugs (e.g., sulfasalazine, sorafenib, and artesunate), which target antioxidant enzyme systems, especially the amino acid antiporter system xcรขยˆย’ and the glutathione peroxidase GPX4. Dysfunctional ferroptosis is implicated in various physiological and pathological processes (e.g., metabolism, differentiation, and immunity). Targeting the ferroptotic network appears to a new treatment option for diseases or pathological conditions (e.g., cancer, neurodegeneration, and ischemia reperfusion injury). While the molecular machinery of ferroptosis remains largely unknown, several transcription factors (e.g., TP53, NFE2L2/NRF2, ATF3, ATF4, YAP1, TAZ, TFAP2C, SP1, HIF1A, EPAS1/HIF2A, BACH1, TFEB, JUN, HIC1, and HNF4A) play multiple roles in shaping ferroptosis sensitivity through either transcription-dependent or transcription-independent mechanisms. In this review, we summarize recent progress in understanding the transcriptional regulation underlying ferroptotic cell death, and discuss how it has provided new insights into cancer therapy.
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      headline:Transcription factors in ferroptotic cell death
      description:Ferroptosis, a form of regulated cell death, is characterized by an excessive degree of iron accumulation and lipid peroxidation. Although it was originally identified only in cells expressing a mutant RAS oncogene, ferroptosis has also been found in normal cells following treatment by small molecules (e.g., erastin and RSL3) or drugs (e.g., sulfasalazine, sorafenib, and artesunate), which target antioxidant enzyme systems, especially the amino acid antiporter system xcรขยˆย’ and the glutathione peroxidase GPX4. Dysfunctional ferroptosis is implicated in various physiological and pathological processes (e.g., metabolism, differentiation, and immunity). Targeting the ferroptotic network appears to a new treatment option for diseases or pathological conditions (e.g., cancer, neurodegeneration, and ischemia reperfusion injury). While the molecular machinery of ferroptosis remains largely unknown, several transcription factors (e.g., TP53, NFE2L2/NRF2, ATF3, ATF4, YAP1, TAZ, TFAP2C, SP1, HIF1A, EPAS1/HIF2A, BACH1, TFEB, JUN, HIC1, and HNF4A) play multiple roles in shaping ferroptosis sensitivity through either transcription-dependent or transcription-independent mechanisms. In this review, we summarize recent progress in understanding the transcriptional regulation underlying ferroptotic cell death, and discuss how it has provided new insights into cancer therapy.
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