IndraLab

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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."