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FGFR2 mutations in bent bone dysplasia syndrome activate nucleolar stress and perturb cell fate determination
Fibroblast Growth Factor (FGF) signaling promotes self-renewal in progenitor cells by encouraging proliferation and inhibiting cellular senescence. Yet, these beneficial effects can be hijacked by disease-causing mutations in FGF receptor (FGFR) during embryogenesis. By studying dominant FGFR2 mutat...
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| Udgivet i: | Hum Mol Genet |
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| Main Authors: | , , , , |
| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
Oxford University Press
2017
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| Fag: | |
| Online adgang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5886181/ https://ncbi.nlm.nih.gov/pubmed/28595297 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/hmg/ddx209 |
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