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MYSM1 activates translation. 8 / 8
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"We have thus far focused on the compromised HSC function due to MYSM1 deficiency causing reduced protein synthesis and increased ferroptosis, as a result."
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"Given that prior studies have shown that HSCs have a characteristically low level of protein synthesis and we have demonstrated how reduced protein synthesis due to MYSM1 loss can induce ferroptosis, we wondered if overexpression of MYSM1 could augment protein synthesis in healthy HSCs and thereby protect the cells from ferroptosis."
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"When cycloheximide (CHX) was applied at specified time points to inhibit protein synthesis, depletion of MYSM1 significantly accelerated ERα degradation and ectopic expression of wild-type MYSM1 plasmid (MYSM1-FL) ameliorated ERα degradation process (Fig. 3C,E)."
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"Another research has reported that the loss of the histone deubiquitinase Myb-Like SWIRM and MPN domains 1 (MYSM1) increased the sensitivity of HSCs to ferroptosis by reducing protein synthesis rates in HSCs [29]."
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"Indeed, the latest evidence suggests that human cord blood HSCs are more susceptible to ferroptosis than downstream progenitor cells ex vivo due to a low level of antioxidant protein synthesis, and MY[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Recently, Zhao et al. demonstrated that histone deubiquitinase MYSM1 (Myb-like, SWIRM and MPN domains 1) deficiency reduced the translation of ferroptosis-protective mRNAs, resulting in increased ferroptosis of human hematopoietic stem cells (HSCs), and HSC population maintenance was fully restored by the ferroptosis inhibitors (e.g., deferoxamine (DFO), ferrostatin-1 (Fer-1), and vitamin E)16."
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"Overall, we demonstrate that the loss of MYSM1 in mouse B cell lymphoma represses the induction of ribosomal protein genes, reduces cellular protein synthesis rate, promotes p53 activation and potently inhibits cMYC oncogenic functions.To compare the location of the genomic binding sites of MYSM1 and cMYC, we consolidated the ChIP‐Seq datasets for cMYC and its dimerization partner MAX from multipotent haematopoietic progenitor cells HPC7 12 , 13 with the MYSM1 ChIP‐Seq acquired in our recent work in a B cell progenitor cell line Ba/F3."
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"In hematopoietic stem cells (HSC), histone deubiquitinase MYSM1 was shown to mediate the vulnerabilities of HSC to ferroptosis stress by regulating protein synthesis."
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