ArticleThe Journal of investigative dermatology2010
Amphiregulin carboxy-terminal domain is required for autocrine keratinocyte growth.
Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci.Nature communications · 2015Pooled it
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- Brigatinib can inhibit proliferation and induce apoptosis of human immortalized keratinocyte cells.Frontiers in pharmacology · 2025Article
- PANoptosis signaling enables broad immune response in psoriasis: From pathogenesis to new therapeutic strategies.Computational and structural biotechnology journal · 2024Article
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- Amphiregulin regulates odontogenic differentiation of dental pulp stem cells by activation of mitogen-activated protein kinase and the phosphatidylinositol 3-kinase signaling pathways.Stem cell research & therapy · 2022Article
- Amphiregulin promotes hair regeneration of skin-derived precursors via the PI3K and MAPK pathways.Cell proliferation · 2021Article
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- Aberrant expression of the UPF1 RNA surveillance gene disturbs keratinocyte homeostasis by stabilizing AREG.International journal of molecular medicine · 2020Article
- Amphiregulin-producing γδ T cells are vital for safeguarding oral barrier immune homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A nonimmune function of T cells in promoting lung tumor progression.The Journal of experimental medicine · 2017Article
- Dual Role of Act1 in Keratinocyte Differentiation and Host Defense: TRAF3IP2 Silencing Alters Keratinocyte Differentiation and Inhibits IL-17 Responses.The Journal of investigative dermatology · 2017Article
- Article
- Article
- Transgenic expression of human amphiregulin in mouse skin: inflammatory epidermal hyperplasia and enlarged sebaceous glands.Experimental dermatology · 2016Article
- Membrane-Tethered Intracellular Domain of Amphiregulin Promotes Keratinocyte Proliferation.The Journal of investigative dermatology · 2016Article
- Epithelial estrogen receptor 1 intrinsically mediates squamous differentiation in the mouse vagina.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Involvement of TNF-α converting enzyme in the development of psoriasis-like lesions in a mouse model.PloS one · 2014Article
- Heparin-binding EGF-like growth factor promotes epithelial-mesenchymal transition in human keratinocytes.The Journal of investigative dermatology · 2012Article
- Genome-wide association study identifies a psoriasis susceptibility locus at TRAF3IP2.Nature genetics · 2010Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
The EGFR ligand amphiregulin (AREG) has been implicated as an important autocrine growth factor in several epithelial malignancies and in psoriasis, a hyperproliferative skin disorder. To characterize the mechanisms by which AREG regulates autocrine epithelial cell growth, we transduced human keratinocytes (KCs) with lentiviral constructs expressing tetracycline (TET)-inducible small hairpin RNA (shRNA). TET-induced expression of AREG shRNA markedly reduced autocrine extracellular signal-regulated kinase phosphorylation, strongly inhibited autocrine KC growth with an efficiency similar to metalloproteinase and EGFR inhibitors, and induced several markers of KC differentiation, including keratins 1 and 10. Addition of various concentrations of exogenous EGFR ligands to KC cultures reversed the growth inhibition in response to AREG-blocking antibodies but not to shRNA-mediated AREG knockdown. Lentivirus-mediated expression of the full-length AREG transmembrane (TM) precursor, but not of the AREG extracellular domain, markedly reversed the shRNA-mediated growth inhibition and morphological changes, and strongly reduced the induction of multiple markers of KC differentiation. Taken together, our data show that autocrine human KC growth is highly dependent on the AREG TM precursor protein and strongly suggest a previously unreported function of the metalloproteinase-processed carboxy (C)-terminal domain of AREG.
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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.