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ChIP-Seq analysis of LCOR and mutated variants lacking the nuclear receptor binding domain or the HTH motif in MDA-MB-231 breast cancer cells

ABSTRACT: ChIP-Seq analysis of LCOR and mutated variants lacking the nuclear receptor binding domain or the HTH motif in MDA-MB-231 breast cancer cells

PROVIDER: PRJNA686061 | ENA |

REPOSITORIES: ENA

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ChIP-Seq analysis of LCOR and mutated variants lacking the nuclear receptor binding domain or the HTH motif in MDA-MB-231 breast cancer cells

Project description:LCOR is a tumor suppressor that induces differentiation of mammary stem cells and cancer stem cells. LCOR orchestrates and sensitizes cells to interferon in ER-negative breast cancer cells. LCOR can act as a co-repressor of activated nuclear receptors and also as a transcription factor by DNA direct binding through its HTH domain. These domains are the most conserved regions of LCOR across vertebrates, suggesting a conserved regulatory function. Here we performed ChiP-seq analysis of LCOR in MDA-MB-231 cells with ectopic expression of the LCOR wild-type, LCOR without the nuclear receptor binding domain (LSKAA) and LCOR with deleted DNA binding domain (HTH). This analysis allows to compare the genome wide distribution of LCOR depending on these specific protein domains

2022-01-04 | GSE163408 | GEO