MYSM1 (Myb Like, SWIRM And MPN Domains 1)

Rescue experiments indicate that inhibiting TRAF2 or TRAF3 can attenuate MYSM1-induced activation of the MAPK pathway. These findings identify MYSM1 as a novel regulator of TRAF2-TRAF3 complex stability and a potential prognostic biomarker and therapeutic target in LUAD.

Hematopoietic stem cell transplantation achieved remission in two patients with adverse cytogenetics. Further research is needed to refine management strategies and assess long-term outcomes in MYSM1-associated marrow failure and MDS.

Furthermore, MYSM1 exacerbated DOX-induced cardiotoxicity by enhancing ferroptosis. This study identified MYSM1 as a potential therapeutic target for DOX-induced cardiotoxicity and illustrated a MYSM1-TRIM21-ferroptosis axis in regulating DOX-induced cardiotoxicity.

The high sequence homology between murine and human MYSM1, along with similar phenotypes observed in Mysm1-deficient models, provides valuable insights into the etiology of human Mysm1-deficiency syndromes. This review aims to offer a foundation for future comprehensive research on MYSM1.

A virtual screen shows that the small molecule Imatinib could potentially interact with catalytic MPN domain of MYSM1 to inhibit BCa cell growth via MYSM1-ERα axis. These findings clarify the molecular mechanism of MYSM1 as an epigenetic modifier in regulation of ERα action and provide a potential therapeutic target for endocrine resistance in BCa.