Identification of ACSL4 as a biomarker and contributor of ferroptosis.

By Hua Yuan, Xuemei Li, Xiu-ying Zhang, R. Kang, D. Tang. Biochemical and Biophysical Research Communications - BBRC, 2016

938 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/cb26ad457fe35ab28b1b0cda7fd195770b815129

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. D. Tang
2. Guido Kroemer
3. R. Kang
4. Xin Chen
5. P. Lei
6. T. Vanden Berghe
7. Peter Vandenabeele
8. Qing-zhang Tuo

In Molecular Biology

1. D. Tang
2. R. Kang
3. Guido Kroemer
4. Xin Chen
5. D. Klionsky
6. Jiao Liu
7. Peter Vandenabeele
8. T. Vanden Berghe

In Pulmonary and Respiratory Medicine

1. D. Tang
2. R. Kang
3. Guido Kroemer
4. Xin Chen
5. D. Klionsky
6. Jiao Liu
7. Jinbao Liu
8. P. Lei

Citations in the corpus

• Regulated cell death (RCD) in cancer: key pathways and targeted therapies (2022, background): “A number of studies have suggested that ACSl4 can be used as a biomarker to predict whether tumor cells can successfully die of iron.(8,365,367) ACSl4 mediated ferroptosis can inhibit the proliferation of glioma cells, so it has the potential to become a new target for glioma treatment.”
• The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. (2017, positive): “In particular, acetyl coenzyme A (acyl-CoA) synthetase long-chain family member 4 (ACSL4) is critical for lipid peroxidation in ferroptotic cell death due to catalyzing esterification of arachidonoyl or adrenoyl into phosphatidylethanolamines (Doll et al., 2017; Kagan et al., 2017; Yuan et al., 2016”
• Autophagy-Dependent Ferroptosis: Machinery and Regulation (2020, background): “The activation of the GPX4, AIFM2, or ESCRT-III pathways can limit or repair the oxidation of PUFAs that result from the activation of the ACSL4-LPCAT3-ALOX pathway.”
• Transferrin Receptor Is a Specific Ferroptosis Marker (2020, neutral): “Acyl-coenzyme A (CoA) synthetase long-chain family member 4 (ACSL4) was found to be required for ferroptotic cell death (Dixon et al., 2015; Doll et al., 2017; Yuan et al., 2016).”
• The Tumor Suppressor Protein p53 and the Ferroptosis Network (2018, positive): “Suppression of ACSL4 expression by RNA interference increases ferroptosis resistance in HepG2 (human hepatoblastoma) and HL-60 (acute myeloid leukemia) cells, whereas overexpression of ACSL4 by gene transfection restores ferroptosis sensitization in LNCaP (a human prostate carcinoma cell line) and K”
• Ferroptosis: mechanisms and links with diseases (2021, background): “In this pathway, it is ACSL4 but not other ACSLs that changes the sensitivity of cells to ferroptosis by affecting the lipid composition,(21) and ACSL4 reduction enhances resistance to ferroptotic cell death.(53) I/R injury, ionizing radiation, and the inhibition of the NF2-YAP pathway can promote f”
• Ferroptosis in infection, inflammation, and immunity (2021, background): “generate AA-CoA (Doll et al., 2017; Kagan et al., 2017; Yuan et al., 2016), which is subsequently incorporated in phospholipid membranes by LPCAT3 (Dixon et al.”
• The interaction between ferroptosis and lipid metabolism in cancer (2020, background): “The PUFA-OOH is the main source of LPO.”