Abstract
Airway stem cells slowly self-renew and produce differentiated progeny to maintain homeostasis throughout the lifespan of an individual. Mutations in the molecular regulators of these processes may drive cancer or degenerative disease, but are also potential therapeutic targets. Conditionally deleting one copy of FGF receptor 2 (FGFR2) in adult mouse airway basal cells results in self-renewal and differentiation phenotypes.We show that FGFR2 signalling correlates with maintenance of expression of a key transcription factor for basal cell self-renewal and differentiation: SOX2. This heterozygous phenotype illustrates that subtle changes in receptor tyrosine kinase signalling can have significant effects, perhaps providing an explanation for the numerous changes seen in cancer.
| Original language | English |
|---|---|
| Pages (from-to) | 1600-1606 |
| Number of pages | 7 |
| Journal | Development (Cambridge) |
| Volume | 144 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 1 May 2017 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Cre-Lox
- Lung
- Mouse
- Progenitor
- Trachea
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Dive into the research topics of 'FGFR2 is required for airway basal cell self-renewal and terminal differentiation'. Together they form a unique fingerprint.Profiles
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Professor Eugenia Piddini
- School of Biochemistry and Biomedical Sciences - Professorial Research Fellow in Cell Biology
- Cancer
Person: Academic , Member
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