ArticleCell discovery2019
STK11 is required for the normal program of ciliated cell differentiation in airways.
Article in Cell discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Variable DPP4 expression in multiciliated cells of the human nasal epithelium as a determinant for MERS-CoV tropism.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Niche-Dependent Regulation of Lkb1 in the Proliferation of Lung Epithelial Progenitor Cells.International journal of molecular sciences · 2022Article
- Review
- LKB1 deficiency upregulates RELM-α to drive airway goblet cell metaplasia.Cellular and molecular life sciences : CMLS · 2021Article
- Novel Approach Combining Transcriptional and Evolutionary Signatures to Identify New Multiciliation Genes.Genes · 2021Article
- Understanding Lung Carcinogenesis from a Morphostatic Perspective: Prevention and Therapeutic Potential of Phytochemicals for Targeting Cancer Stem Cells.International journal of molecular sciences · 2021Review
- The transcriptional landscape of the cultured murine middle ear epithelium in vitro.Biology open · 2021Article
- Consecutive Hypoxia Decreases Expression ofFrontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The functional properties of mucosal surfaces are dependent on establishing the correct proportions of specialized epithelial cell types. Multiciliated cells (also known as ciliated cells) are evolutionarily conserved and functionally indispensable epithelial cells, as suggested by the link between ciliated cell dysfunction and chronic human disease. Ciliated cell differentiation is an ordered process that involves initial cell fate determination and multiciliogenesis. STK11, a serine/threonine kinase, has been reported to be downregulated in human diseases associated with ciliopathies and functions as a tumor suppressor. Here, we show that STK11 is a physiological factor for the normal program of ciliated cell differentiation by phosphorylating MARK3, which directly suppresses ERK1/2 mediated pRB inactivation. Loss of
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Registered trials
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