ArticleOncogene2010
c-Abl regulates estrogen receptor alpha transcription activity through its stabilization by phosphorylation.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- ChIP happens: from biochemical origins to the modern omics toolbox for understanding steroid hormone receptors.The Biochemical journal · 2026Review
- Long-Chain Fatty Acids Alter Estrogen Receptor Expression in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Monopolar spindle 1 contributes to tamoxifen resistance in breast cancer through phosphorylation of estrogen receptor α.Breast cancer research and treatment · 2023Article
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- A novel polypeptide encoded by the circular RNA ZKSCAN1 suppresses HCC via degradation of mTOR.Molecular cancer · 2023Article
- Decoding the Therapeutic Implications of the ERα Stability and Subcellular Distribution in Breast Cancer.Frontiers in endocrinology · 2022Review
- Review
- C1222C Deletion in Exon 8 ofFrontiers in oncology · 2020Article
- Hypoxia differentially regulates estrogen receptor alpha in 2D and 3D culture formats.Archives of biochemistry and biophysics · 2019Article
- RNF34 functions in immunity and selective mitophagy by targeting MAVS for autophagic degradation.The EMBO journal · 2019Article
- Article
- EnABLing Tumor Growth and Progression: Recent progress in unraveling the functions of ABL kinases in solid tumor cells.Current pharmacology reports · 2018Article
- Polyubiquitination inhibition of estrogen receptor alpha and its implications in breast cancer.World journal of clinical oncology · 2018Review
- SMURF1 facilitates estrogen receptor ɑ signaling in breast cancer cells.Journal of experimental & clinical cancer research : CR · 2018Article
- Targeting BCR-ABL+ stem/progenitor cells and BCR-ABL-T315I mutant cells by effective inhibition of the BCR-ABL-Tyr177-GRB2 complex.Oncotarget · 2017Article
- ERRα negatively regulates type I interferon induction by inhibiting TBK1-IRF3 interaction.PLoS pathogens · 2017Article
- c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression.Oncotarget · 2016Article
- ChIP-seq predicted estrogen receptor biding sites in human breast cancer cell line MCF7.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Elevated expression of TANK-binding kinase 1 enhances tamoxifen resistance in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptors are members of the steroid hormone superfamily of nuclear receptors that act as ligand-activated transcription factors. Similar to other steroid hormone receptors, estrogen receptor alpha (ERalpha) is a substrate for protein kinases, and phosphorylation has profound effects on the function of this receptor. In this study, we show that ERalpha associates with c-Abl nonreceptor tyrosine kinase. The direct interaction is mediated by two PXXP motifs of ERalpha and the c-Abl SH3 domain. Mutational analysis and in vitro kinase assays show that ERalpha can be phosphorylated on two sites, tyrosine 52 (Y-52) and tyrosine 219 (Y-219). ERalpha phosphorylation by c-Abl stabilizes ERalpha, resulting in enhanced ERalpha transcriptional activity and increased expression of endogenous ERalpha target genes. Furthermore, ERalpha phosphorylation at the Y-219 site affects DNA binding and dimerization by ERalpha. Both the c-Abl inhibitor and the c-Abl kinase dead mutation abolish the c-Abl-induced accumulation of ERalpha and enhancement of ERalpha transcriptional activity, indicating that c-Abl kinase activity is required for regulation of the ERalpha function. Moreover, the ERalpha (Y52,219F) mutant shows reduced breast cancer cell growth and invasion. Taken together, these results show that c-Abl is a novel kinase that upregulates ERalpha expression and promotes breast cancer cell proliferation, suggesting a great potential for this kinase to function as a therapeutic target for breast cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.