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Xinxin Song

Researcher at University of Pittsburgh

Publications -  35
Citations -  5122

Xinxin Song is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Apoptosis & Autophagy. The author has an hindex of 19, co-authored 31 publications receiving 2758 citations. Previous affiliations of Xinxin Song include University of Texas Southwestern Medical Center & Peking Union Medical College.

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Ferroptosis: process and function.

TL;DR: Misregulated ferroptosis has been implicated in multiple physiological and pathological processes, including cancer cell death, neurotoxicity, neurodegenerative diseases, acute renal failure, drug-induced hepatotoxicity, hepatic and heart ischemia/reperfusion injury, and T-cell immunity.
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Autophagy promotes ferroptosis by degradation of ferritin

TL;DR: It is demonstrated that autophagy contributes to ferroptosis by degradation of ferritin in fibroblasts and cancer cells by knocking out or knockdown of Atg5 and Atg7, which provides novel insight into the interplay between Autophagy and regulated cell death.
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The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity

TL;DR: Findings reveal a direct molecular link between TP53 and DPP4 in the control of lipid metabolism and may provide a precision medicine strategy for the treatment of colorectal cancer by induction of ferroptosis.
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AMPK-Mediated BECN1 Phosphorylation Promotes Ferroptosis by Directly Blocking System Xc- Activity.

TL;DR: It is shown that BECN1 plays a hitherto unsuspected role in promoting ferroptosis through directly blocking system Xc- activity via binding to its core component, SLC7A11 (solute carrier family 7 member 11).
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Role of the IL-6-JAK1-STAT3-Oct-4 pathway in the conversion of non-stem cancer cells into cancer stem-like cells

TL;DR: The results imply that removing CSCs may prompt non-CSCs in the tumor to convert into stem cells to maintain the equilibrium, and suggest that the IL-6-JAK1-STAT3 signal transduction pathway plays an important role in the conversion of non-cSCs into C SCs through regulation of OCT-4 gene expression.