RAS–RAF–MEK-dependent oxidative cell death involving voltage-dependent anion channels

By Nicholas Yagoda, Moritz von Rechenberg, Elma Zaganjor, Andras J. Bauer, W. Yang, Daniel J. Fridman, Adam J. Wolpaw, I. Smukste, J. Peltier, J. Boniface and 4 more. Nature, 2007

1,483 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/09ecea78c3334afe3711fa38ffdfef572ffab25d

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Citations in the corpus

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. (2017, neutral): “Cells dying by ferroptosis primarily exhibit shrunken and damaged mitochondria by electron microscopy, with few other morphological changes evident prior to the point of cell death (Yagoda et al., 2007).”
Synchronized renal tubular cell death involves ferroptosis (2014, methodology): “Because we previously reported a beneficial effect of the secondgeneration ferrostatin 11-92 (29) in a model of acute injury of freshly isolated renal tubules, we looked for the morphology of such tubules in the presence of erastin, a well-described inducer of ferroptosis, a necrotic type cell death”
The cell biology of ferroptosis (2024, neutral): “In cells treated with the system x c– inhibitor erastin, mitochondria are smaller, with disorganized cristae 1,80 .”
Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications. (2022, neutral): “, 2003) that depended on the accumulation of oxidative stress and cellular iron levels (Yagoda et al., 2007).”
Oxidative Stress in Cancer (2020, background): “For example, erastin is a small-molecule modulator of voltage-dependent anion channels (VDAC2/VDAC3) (Yagoda et al., 2007) and of the GSH transporter xCT (Dixon et al.”