@article{d175f45feba94f57ace69089ada077b4,
title = "Apoptosis, axonal growth defects, and degeneration of peripheral neurons in mice lacking CREB",
abstract = "CRE-binding protein (CREB) belongs to a family of transcription factors that mediates stimulus-dependent gene expression in neuronal and non-neuronal cells. Here we show that CREB is phosphorylated on its transcriptional regulatory site, Ser-133, in vivo in a neurotrophin-dependent manner. In mice harboring a null mutation in the Creb gene, sensory neurons exhibit excess apoptosis and degeneration, and display impaired axonal growth and projections. Interestingly, excess apoptosis is not observed in the central nervous system. CREB is required within sensory and sympathetic neurons for survival and axon extension since both of these neurotrophin-dependent processes are compromised in cultured neurons from CREB null mice. Thus, during their period of neurotrophin dependency, peripheral neurons require CREB-mediated gene expression for both survival and growth in vivo.",
author = "Lonze, {Bonnie E.} and Antonella Riccio and Sonia Cohen and Ginty, {David D.}",
note = "Funding Information: We thank Dr. Sohyun Ahn for discussions and help with mouse husbandry during initial stages of the project. We are grateful to Dr. Alex Kolodkin and members of the Ginty laboratory for helpful discussions, and we thank Dr. Mark Grimes and Dr. Jeroen Pasterkamp for insightful comments on this manuscript. We also thank Pat Wilcox for preparation of paraffin sections, Dr. Roman Giger and Dr. Hideki Enomoto for advice about whole-mount immunostaining, Dr. Richelle Strom for help with photography, and Dr. Debby R.S. Cohen for offering invaluable suggestions for BrdU immunostaining. Dr. Louis Reichardt generously provided the anti-TrkA antibody. CREB mutant mice were provided by Dr. G{\"u}nther Sch{\"u}tz and the Deutsches Krebsforschungszentrum, and Bax mutant mice were provided by Dr. William Snider. We are indebted to Dr. Julie Blendy for advice with the mouse colony and genotyping. This work was supported by National Institutes of Health grant NS34814 (D.D.G.) and the Medical Scientist Training Program (B.E.L.). David Ginty is an Assistant Investigator of the Howard Hughes Medical Institute.",
year = "2002",
month = apr,
day = "25",
doi = "10.1016/S0896-6273(02)00686-4",
language = "English (US)",
volume = "34",
pages = "371--385",
journal = "Neuron",
issn = "0896-6273",
publisher = "Cell Press",
number = "3",
}