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STAT1 binds MYSM1. 15 / 15
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"Besides, we found that oeMYSM1 only promoted the mRNA expression of necroptosis-related genes ( Mlkl / Ripk3 ) rather than other PCD-related genes ( Ripk1 / Fas / Zbp1 / Casp3 ) in H/R-induced HL-1 cells ( xref B-G), indicating that MYSM1-STAT1 axis up-regulated the transcription and expression of necroptosis-related genes."
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"These findings confirmed a direct interaction between MYSM1 and STAT1, suggesting that STAT1 may be a crucial substrate protein of MYSM1."
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"These data indicated that MYSM1 interacts with STAT1 through the SWIRM domain and deubiquitinates STAT1 through the MPN domain."
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"In conclusion, this study illustrated a MYSM1-STAT1 axis in regulating myocardial I/R injury and identified MYSM1 as a pharmacological target for myocardial I/R injury."
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"Therefore, we speculated that MYSM1 may utilize STAT1 as a crucial substrate in the regulation of myocardial I/R injury.Then we examined the direct interaction between MYSM1 and STAT1."
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"These findings confirmed a direct interaction between MYSM1 and STAT1, suggesting that STAT1 may be a crucial substrate protein of MYSM1."
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"Consistently, our data showed that MYSM1 binds to STAT1 mainly through the SWIRM domain."
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"In this study, we demonstrated a specific MYSM1-STAT1 axis in myocardial I/R injury, which might avoid the side effects of targeting STAT1 alone, indicating that targeting MYSM1 could be a more specific therapeutic strategy for myocardial I/R injury."
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"Apart from the MYSM1-STAT1 interaction, MYSM1 has been reported to deubiquitinate other substrate proteins xref , such as E2A xref , GATA2 xref , and histone H2A xref ."
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"Then we examined the direct interaction between MYSM1 and STAT1."
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"We also demonstrated the pathogenic role of specific MYSM1-STAT1 axis in myocardial I/R injury, suggesting that small molecule compounds targeting MYSM1 may be an attractive therapeutic strategy for this condition."
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"The binding of endogenous MYSM1 and STAT1 was observed in myocardial I/R injury (Figure xref F) and H/R-induced HL-1 cells (Figure xref G)."
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"To determine the domain required for MYSM1-STAT1 interaction, we co-transfected NIH/3T3 cells with Myc-STAT1, Flag-MYSM1 (MYSM1-WT) or its mutants lacking SANT domain (△SANT), SWIRM domain (△SWIRM), or MPN domain (△MPN) (Figure xref F)."
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"As depicted inFigure xref G, STAT1 interacted with MYSM1-WT, MYSM1-△SANT, and MYSM1-△MPN, but failed to bind to MYSM1-△SWIRM, indicating that MYSM1 binds to STAT1 through the SWIRM domain."
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"Conclusion: This study illustrated a MYSM1-STAT1 axis in regulating myocardial I/R injury and identified MYSM1 as a pharmacological target for myocardial I/R injury."
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