Nuclear localization of EGF receptor and its potential new role as a transcription factor
By Shiaw-Yih Lin, K. Makino, W. Xia, A. Matin, Y. Wen, K. Kwong, L. Bourguignon, M. Hung. Nature Cell Biology, 2001
1,119 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d80eddca3bebe4e1572e9ac92efdb4b4c1a57bf9
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Citations in the corpus
- Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “it has been shown that nuclear EGFR aids in the transcription of important cell cycle progression mediators, including CYCLIN D1 and c-MYC, among other proto-oncogenes [354,370].”
- The molecular biology of head and neck cancer (2011, background): “Most intriguingly, EGF-bound EGFR is also able to translocate to the nucleus and it functions as a transcription factor or co-activator of other transcription factors, such as signal transducer and activator of transcription (STAT) protein”
- The epidermal growth factor receptor family: Biology driving targeted therapeutics (2008, background): “EGFR has been proposed as a transcription factor as localization to the nucleus is associated with increased CyclinD1 expression [64].”
- Automated subcellular localization and quantification of protein expression in tissue microarrays (2002, background): “In addition, recent studies have shown that membrane-bound growth factor receptors (for example, epidermal growth factors, EGFR and ERB-B4, and fibroblast growth factor) can translocate to the nucleus and may act as transcriptional regulator”
- Targets of curcumin (2011, background): “It has also been shown that the EGFR can translocate to the nucleus, where it can act as a transcription factor for cyclin D1 [65,68] and as a co-activator for STAT3 [69] and E2F1 [70].”
- Targeting the EGFR signaling pathway in cancer therapy (2012, background): “It is also proposed that the nuclear import of EGFR regulates gene expression by binding to an AT-rich sequence of the target gene’s promoter [31,39].”
- PD-L1-Mediated Gasdermin C Expression Switches Apoptosis to Pyroptosis in Cancer Cells and Facilitates Tumor Necrosis (2020, background): “The N-terminal domain (1-365) of GSDMC is sufficient to induce pyroptosis (a) 3-D structural modeling of GSDMC.”
- Epidermal growth factor receptor cooperates with signal transducer and activator of transcription 3 to induce epithelial-mesenchymal transition in cancer cells via up-regulation of TWIST gene expression. (2007, methodology): “This procedure was done as described previously (24, 32).”