A HuD-ZBP1 ribonucleoprotein complex localizes GAP-43 mRNA into axons through its 3′ untranslated region AU-rich regulatory element
Version of Record online: 30 APR 2013
© 2013 International Society for Neurochemistry
Journal of Neurochemistry
Volume 126, Issue 6, pages 792–804, September 2013
How to Cite
J. Neurochem. (2013) 126, 792–804.
- Issue online: 6 SEP 2013
- Version of Record online: 30 APR 2013
- Accepted manuscript online: 15 APR 2013 07:30AM EST
- Manuscript Revised: 1 APR 2013
- Manuscript Accepted: 1 APR 2013
- Manuscript Received: 31 OCT 2012
- NIH. Grant Numbers: P20GM103464, R01-NS41596, R01-NS30255
- Craig H. Neilsen Foundation. Grant Number: 124124
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
Figure S1. Schematics of constructs that are used in the study.
Figure S2. Axotomy triggers an increase in axonal GAP-43 mRNA levels that reduce axonal β -actin mRNA.
Figure S3. Sequences in the 3′UTR of GAP-43 support reporter mRNA translation in axons.
Figure S4. Both localizing and non-localizing reporter mRNAs are expressed in cell body of neurons.
Figure S5. Over-expression of GAP-43′s 3′UTR attenuates axon outgrowth when the ARE is included.
Figure S6. Over-expression of axonally targeted GAP-43 ORF increases axonal growth when the ARE is included.
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.