Musashi: a translational regulator of cell fate
Open Access
- 1 April 2002
- journal article
- review article
- Published by The Company of Biologists in Journal of Cell Science
- Vol. 115 (7) , 1355-1359
- https://doi.org/10.1242/jcs.115.7.1355
Abstract
Transcription is thought to have a major role in the regulation of cell fate; the importance of translational regulation in this process has been less certain. Recent findings demonstrate that translational regulation contributes to cell-fate specification. The evolutionarily conserved, neural RNA-binding protein Musashi, for example, controls neural cell fate. The protein functions in maintenance of the stem-cell state, differentiation, and tumorigenesis by repressing translation of particular mRNAs. In mammals it might play an important role in activating Notch signalling by repressing translation of the Notch inhibitor m-Numb.Keywords
This publication has 41 references indexed in Scilit:
- The Neural RNA-Binding Protein Musashi1 Translationally Regulates Mammalian numb Gene Expression by Interacting with Its mRNAMolecular and Cellular Biology, 2001
- Notch Signaling: Cell Fate Control and Signal Integration in DevelopmentScience, 1999
- CONTROL OF TRANSLATION INITIATION IN ANIMALSAnnual Review of Cell and Developmental Biology, 1998
- Fibroblast growth factor‐2/brain‐derived neurotrophic factor—associated maturation of new neurons generated from adult human subependymal cellsAnnals of Neurology, 1998
- Control of Daughter Cell Fates during Asymmetric Division: Interaction of Numb and NotchNeuron, 1996
- Musashi, a neural RNA-binding protein required for drosophila adult external sensory organ developmentNeuron, 1994
- Asymmetric distribution of numb protein during division of the sensory organ precursor cell confers distinct fates to daughter cellsCell, 1994
- hnRNP PROTEINS AND THE BIOGENESIS OF mRNAAnnual Review of Biochemistry, 1993
- Sex in flies: the splice of lifeNature, 1989
- numb, a gene required in determination of cell fate during sensory organ formation in Drosophila embryosCell, 1989