IndraLab

Statements

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"Here, we performed an IP combined with LC-MS/MS analysis and identified TRIM21 as a direct substrate protein of MYSM1 in DOX-induced cardiotoxicity."
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"In this study, we aimed to explore the function and regulatory mechanisms of MYSM1 in DOX-induced cardiotoxicity."
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"Furthermore, MYSM1 exacerbated DOX-induced cardiotoxicity by enhancing ferroptosis."
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"MYSM1 mediates ferroptosis in DOX-induced cardiotoxicity."
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"In this research, through a comparison of RNA sequencing (RNA-seq) databases and functional screening of the JAMMs, we identified Myb-like, SWIRM, and MPN domains 1 (MYSM1) as a potential regulator of DOX-induced cardiotoxicity."
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"Up to now, the potential role and mechanism of MYSM1 in DOX-induced cardiotoxicity have not yet been revealed.The purpose of this study was to clarify MYSM1’s regulatory function and mechanism in DOX-induced cardiotoxicity."
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"Furthermore, MYSM1 exacerbated DOX-induced cardiotoxicity by increasing ferroptosis signaling pathway activity."
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"To further verify the involvement of ferroptosis in MYSM1-mediated DOX-induced cardiotoxicity, the ferroptosis inhibitor ferrostatin-1 (Fer-1) was administered to HL-1 cells before DOX treatment."
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"PI staining confirmed that the ferroptosis inhibitor Fer-1 alleviated the cardiotoxicity induced by MYSM1 overexpression (Fig. 7Q-R)."
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"Identification of MYSM1 as a regulator of DOX-induced cardiotoxicity."
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