PUBLICATION
FK506-binding protein 5 regulates cell quiescence-proliferation decision in zebrafish epithelium
- Authors
- Li, Y., Liu, C., Bai, X., Li, M., Duan, C.
- ID
- ZDB-PUB-230601-45
- Date
- 2023
- Source
- FEBS letters 597(14): 1868-1879 (Journal)
- Registered Authors
- Duan, Cunming, Li, Mingyu
- Keywords
- Akt, FK506 binding protein 5, IGF signaling, calcium signaling, cell cycle, ionocyte
- MeSH Terms
-
- Animals
- Cell Proliferation
- Epithelium/metabolism
- Proto-Oncogene Proteins c-akt*/genetics
- Proto-Oncogene Proteins c-akt*/metabolism
- Tacrolimus Binding Proteins/genetics
- Tacrolimus Binding Proteins/metabolism
- Zebrafish*/genetics
- Zebrafish*/metabolism
- PubMed
- 37259581 Full text @ FEBS Lett.
Citation
Li, Y., Liu, C., Bai, X., Li, M., Duan, C. (2023) FK506-binding protein 5 regulates cell quiescence-proliferation decision in zebrafish epithelium. FEBS letters. 597(14):1868-1879.
Abstract
Using a zebrafish ionocyte model, transcriptomics and genetic analyses were performed to identify pathways and genes involved in cell quiescence-proliferation regulation. GO and KEGG pathway analyses revealed that genes involved in transcription regulation, cell cycle, Foxo signaling, and Wnt signaling pathway are enriched among the up-regulated genes, while those involved in ion transport, cell adhesion, and oxidation-reduction are enriched among the down-regulated genes. Among the top up-regulated genes is FK506-binding protein 5 (Fkbp5). Genetic deletion and pharmacological inhibition of Fkbp5 abolished ionocyte reactivation and impaired Akt signaling. Forced expression of a constitutively active form of Akt rescued the defects caused by Fkbp5 inhibition. These results uncover a key role of Fbkp5 in regulating the quiescence-proliferation decision via Akt signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping