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Cells ; 10(3)2021 03 11.
Article in English | MEDLINE | ID: mdl-33799807

ABSTRACT

ADP-ribosylation is a post-translational protein modification catalyzed by a family of proteins known as poly-ADP-ribose polymerases. PARP7 (TIPARP; ARTD14) is a mono-ADP-ribosyltransferase involved in several cellular processes, including responses to hypoxia, innate immunity and regulation of nuclear receptors. Since previous studies suggested that PARP7 was regulated by 17ß-estradiol, we investigated whether PARP7 regulates estrogen receptor α signaling. We confirmed the 17ß-estradiol-dependent increases of PARP7 mRNA and protein levels in MCF-7 cells, and observed recruitment of estrogen receptor α to the promoter of PARP7. Overexpression of PARP7 decreased ligand-dependent estrogen receptor α signaling, while treatment of PARP7 knockout MCF-7 cells with 17ß-estradiol resulted in increased expression of and recruitment to estrogen receptor α target genes, in addition to increased proliferation. Co-immunoprecipitation assays revealed that PARP7 mono-ADP-ribosylated estrogen receptor α, and mass spectrometry mapped the modified peptides to the receptor's ligand-independent transactivation domain. Co-immunoprecipitation with truncated estrogen receptor α variants identified that the hinge region of the receptor is required for PARP7-dependent mono-ADP-ribosylation. These results imply that PARP7-mediated mono-ADP-ribosylation may play an important role in estrogen receptor positive breast cancer.


Subject(s)
ADP-Ribosylation , Breast Neoplasms/enzymology , Cell Proliferation , Estrogen Receptor alpha/metabolism , Poly(ADP-ribose) Polymerases/metabolism , ADP-Ribosylation/drug effects , Breast Neoplasms/genetics , Breast Neoplasms/pathology , Cell Proliferation/drug effects , Estrogen Receptor alpha/agonists , Estrogen Receptor alpha/genetics , Estrogens/pharmacology , Female , Gene Expression Regulation, Neoplastic , Humans , MCF-7 Cells , Neoplasm Proteins/genetics , Neoplasm Proteins/metabolism , Nucleoside Transport Proteins , Poly(ADP-ribose) Polymerase Inhibitors/pharmacology , Poly(ADP-ribose) Polymerases/genetics , Signal Transduction
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