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Expression data of cultured MCF10A cells transduced with MYB or MYB-NFIB expression vectors

ABSTRACT: Expression data of cultured MCF10A cells transduced with MYB or MYB-NFIB expression vectors

PROVIDER: PRJNA561286 | ENA |

REPOSITORIES: ENA

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Expression data of cultured MCF10A cells transduced with MYB or MYB-NFIB expression vectors

Project description:This experiment investigates differences between control cells (empty vector) and cells with MYB or MYB-NFIB (M14N9) overexpression using MSCV vectors

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RNA-seq of MCF10A transduced with an inducible lentiviral MYB expression system

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Expression data after knockdown of MYB-NFIB and IGF1R/INSR inhibition in ACC cells

Project description:The MYB-NFIB gene is a driver-mutation in the majority of adenoid cystic carcinomas (ACCs) and believed to control a large number of genes involved in tumorigenesis. This experiment investigates the effects on gene expression after siRNA knock-down of MYB-NFIB and/or inhibition of IGF1R/INSR signaling in ACC cells.

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RNA-seq on MCF10A-YAP5SA cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting the TEAD4 binding motif within the identified enhancers

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RNA-seq of MCF10A transduced with an inducible lentiviral MYB expression system

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RNA-seq on MCF10A-YAP cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting TRAM2 gene

Project description:RNA-seq on MCF10A-YAP cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting TRAM2 gene

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RNA-seq on MCF10A-YAP cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting TRAM2 gene

Project description:We performed a CRISPR-based functional genetic screen targeting TEAD4 binding motif located within the YAP-bound enhancers. The screen identified a novel enhancer regulating TRAM2. We observed TRAM2 overexpression can induce EMT as YAP does. Then, we performed the RNA-seq to measure the transcription changes upon TRAM2-KOs in MCF10A-YAP cells

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MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

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Myb specificity determinants

Project description:Recombinant adenovirus vectors were used to express wild type or domain swap mutants of A-Myb and c-Myb transcription factors in MCF-7 cells or pimary lung epithelial cells or fibroblasts. The results show that Myb proteins have extreme context specificity and identify sub-domains responsible for the activation of specific sets of target genes. Keywords = Myb proteins Keywords = oncogenes Keywords = transcription Keywords = gene activation Keywords: ordered

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Gene expression changes upon expression of activated versions of MEK1 and HRAS in MCF10A cells

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