Vladimir A. Tyurin

Corrigendum to: Mitochondrial bioenergetics and cardiolipin remodeling abnormalities in mitochondrial trifunctional protein deficiency

Endoplasmic reticulum–mitochondria contacts are prime hotspots of phospholipid peroxidation driving ferroptosis

Antiferroptotic Drugs Reduce sFlt-1 Release and Placenta Damage in Preeclampsia

Antiferroptotic Drugs Reduce sFlt-1 Release and Placenta Damage in Preeclampsia.

Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression.

Figure S3 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S6 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Table S3 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S1 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S4 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Table S2 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S8 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S9 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S2 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S7 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Table S1 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S10 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Data from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

Figure S5 from Targeting LxCxE Cleft Pocket of Retinoblastoma Protein in Immunosuppressive Macrophages Inhibits Ovarian Cancer Progression

PHLDA2-mediated phosphatidic acid peroxidation triggers a distinct ferroptotic response during tumor suppression

Strikingly High Activity of 15‐Lipoxygenase Towards Di‐Polyunsaturated Arachidonoyl/Adrenoyl‐Phosphatidylethanolamines Generates Peroxidation Signals of Ferroptotic Cell Death

Strikingly High Activity of 15-Lipoxygenase Towards Di-Polyunsaturated Arachidonoyl/Adrenoyl-Phosphatidylethanolamines Generates Peroxidation Signals of Ferroptotic Cell Death.

Ferroptosis of select skin epithelial cells initiates and maintains chronic systemic immune-mediated psoriatic disease

Mitochondrial bioenergetics and cardiolipin remodeling abnormalities in mitochondrial trifunctional protein deficiency

Strikingly High Activity of 15‐Lipoxygenase Towards Di‐Polyunsaturated Arachidonoyl/Adrenoyl‐Phosphatidylethanolamines Generates Peroxidation Signals of Ferroptotic Cell Death

Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression.

Redox phospholipidomics discovers pro-ferroptotic death signals in A375 melanoma cells in vitro and in vivo.

Melanoma-associated repair-like Schwann cells suppress anti-tumor T-cells via 12/15-LOX/COX2-associated eicosanoid production.

Formation of protein adducts with Hydroperoxy-PE electrophilic cleavage products during ferroptosis.

Discovering selective antiferroptotic inhibitors of the 15LOX/PEBP1 complex noninterfering with biosynthesis of lipid mediators.