Quantitative transcriptional control of ErbB receptor signaling undergoes graded to biphasic response for cell differentiation - PubMed (original) (raw)
. 2007 Feb 9;282(6):4045-56.
doi: 10.1074/jbc.M608653200. Epub 2006 Dec 1.
Affiliations
- PMID: 17142811
- DOI: 10.1074/jbc.M608653200
Free article
Quantitative transcriptional control of ErbB receptor signaling undergoes graded to biphasic response for cell differentiation
Takeshi Nagashima et al. J Biol Chem. 2007.
Free article
Erratum in
- J Biol Chem. 2014 Jul 25;289(30):20491
Abstract
ErbB receptor ligands, epidermal growth factor (EGF) and heregulin (HRG), induce dose-dependent transient and sustained intracellular signaling, proliferation, and differentiation of MCF-7 breast cancer cells, respectively. In an effort to delineate the ligand-specific cell determination mechanism, we investigated time course gene expressions induced by EGF and HRG that induce distinct cellular phenotypes in MCF-7 cells. To analyze independently the effects of ligand dosage and time for gene expression, we developed a statistical method for estimating the two effects. Our results indicated that signal transduction pathways convey quantitative properties of the dose-dependent activation of ErbB receptor to early transcription. The results also implied that moderate changes in the expression levels of a number of genes, not the predominant regulation of a few specific genes, might cooperatively work at the early stage of the transcription for determining cell fate. However, the EGF- and HRG-induced distinct signal durations resulted in the ligand-oriented biphasic induction of proteins after 20 min. The selected gene list and HRG-induced prolonged signaling suggested that transcriptional feedback to the intracellular signaling results in a graded to biphasic response in the cell determination process and that each ErbB receptor is inextricably responsible for the control of amplitude and duration of cellular biochemical reactions.
Similar articles
- Epidermal growth factor receptor, c-erbB2 and c-erbB3 receptor interaction, and related cell cycle kinetics of SK-BR-3 and BT474 breast carcinoma cells.
Brockhoff G, Heiss P, Schlegel J, Hofstaedter F, Knuechel R. Brockhoff G, et al. Cytometry. 2001 Aug 1;44(4):338-48. doi: 10.1002/1097-0320(20010801)44:4<338::aid-cyto1125>3.0.co;2-v. Cytometry. 2001. PMID: 11500850 - Signaling molecules implicated in heregulin induction of growth arrest and apoptosis.
Guerra-Vladusic FK, Vladusic EA, Tsai MS, Lupu R. Guerra-Vladusic FK, et al. Oncol Rep. 2001 Nov-Dec;8(6):1203-14. doi: 10.3892/or.8.6.1203. Oncol Rep. 2001. PMID: 11605034 - Modular anti-EGFR and anti-Her2 targeting of SK-BR-3 and BT474 breast cancer cell lines in the presence of ErbB receptor-specific growth factors.
Diermeier-Daucher S, Breindl S, Buchholz S, Ortmann O, Brockhoff G. Diermeier-Daucher S, et al. Cytometry A. 2011 Sep;79(9):684-93. doi: 10.1002/cyto.a.21107. Epub 2011 Jul 22. Cytometry A. 2011. PMID: 21786419 - Essential role for Rac in heregulin beta1 mitogenic signaling: a mechanism that involves epidermal growth factor receptor and is independent of ErbB4.
Yang C, Liu Y, Lemmon MA, Kazanietz MG. Yang C, et al. Mol Cell Biol. 2006 Feb;26(3):831-42. doi: 10.1128/MCB.26.3.831-842.2006. Mol Cell Biol. 2006. PMID: 16428439 Free PMC article. - Robustness analysis of the detailed kinetic model of an ErbB signaling network by using dynamic sensitivity.
Masunaga H, Sugimoto Y, Magi S, Itasaki R, Okada-Hatakeyama M, Kurata H. Masunaga H, et al. PLoS One. 2017 May 24;12(5):e0178250. doi: 10.1371/journal.pone.0178250. eCollection 2017. PLoS One. 2017. PMID: 28542548 Free PMC article.
Cited by
- Self-organization of whole-gene expression through coordinated chromatin structural transition.
Zimatore G, Tsuchiya M, Hashimoto M, Kasperski A, Giuliani A. Zimatore G, et al. Biophys Rev (Melville). 2021 Sep 21;2(3):031303. doi: 10.1063/5.0058511. eCollection 2021 Sep. Biophys Rev (Melville). 2021. PMID: 38505632 Free PMC article. Review. - Growth factor-induced activation of MSK2 leads to phosphorylation of H3K9me2S10 and corresponding changes in gene expression.
Wong KG, Cheng YF, Wu VH, Kiseleva AA, Li J, Poleshko A, Smith CL, Epstein JA. Wong KG, et al. Sci Adv. 2024 Mar 15;10(11):eadm9518. doi: 10.1126/sciadv.adm9518. Epub 2024 Mar 13. Sci Adv. 2024. PMID: 38478612 Free PMC article. - From Cell States to Cell Fates: Control of Cell State Transitions.
Tsuchiya M, Giuliani A, Brazhnik P. Tsuchiya M, et al. Methods Mol Biol. 2024;2745:137-162. doi: 10.1007/978-1-0716-3577-3_9. Methods Mol Biol. 2024. PMID: 38060184 - Synchronization between Attractors: Genomic Mechanism of Cell-Fate Change.
Tsuchiya M, Brazhnik P, Bizzarri M, Giuliani A. Tsuchiya M, et al. Int J Mol Sci. 2023 Jul 18;24(14):11603. doi: 10.3390/ijms241411603. Int J Mol Sci. 2023. PMID: 37511359 Free PMC article. Review. - Design principles of improving the dose-response alignment in coupled GTPase switches.
Qiao L, Ghosh P, Rangamani P. Qiao L, et al. NPJ Syst Biol Appl. 2023 Jan 31;9(1):3. doi: 10.1038/s41540-023-00266-9. NPJ Syst Biol Appl. 2023. PMID: 36720885 Free PMC article.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous