Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene regulation by phosphomimetic Myc (MycD), cytosine arabinoside (AraC) and retinoic acid (RA)


ABSTRACT: We aimed to investigate whether the previously observed synergistic effects of AraC and RA in stimulating leukemia differentiation could be at least partially dependent on Pak2-mediated phosphorylation of Myc. Genome-wide analysis of NB4 cells treated with RA, AraC with RA, or MycD with RA revealed a significant 60% overlap between RA-target genes superactivated by AraC with RA, or MycD with RA, with respect to RA alone. NB4 cells infected with ER-tagged inducible empty vector (CTL), MycD or MycA were treated with 4-OHT (200 nM, 16 h) to induce MycD-ER and MycA-ER expression. CTL cells were either vehicle or AraC (25 μM) treated for 16 h. Short treatment of RA (10 nM, 4 h) was performed in CTL, AraC and MycD-expressing cells. Four biologically independent experiments were performed at each time.

ORGANISM(S): Homo sapiens

SUBMITTER: Luciano Di Croce 

PROVIDER: E-GEOD-29213 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MYC proto-oncogene is a key player in cell homeostasis that is commonly deregulated in human carcinogenesis(1). MYC can either activate or repress target genes by forming a complex with MAX (ref. 2). MYC also exerts MAX-independent functions that are not yet fully characterized(3). Cells possess an intrinsic pathway that can abrogate MYC-MAX dimerization and E-box interaction, by inducing phosphorylation of MYC in a PAK2-dependent manner at three residues located in its helix-loop-helix domain(4  ...[more]

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