CREB activity maintains the survival of cingulate cortical pyramidal neurons in the adult mouse brain.

Molecular Pain
Hushan AoMin Zhuo

Abstract

Cyclic AMP-responsive element binding protein (CREB) activity is known to contribute to important neuronal functions, such as synaptic plasticity, learning and memory. Using a microelectroporation technique to overexpress dominant negative mutant CREB (mCREB) in the adult mouse brain, we found that overexpression of mCREB in the forebrain cortex induced neuronal degeneration. Our findings suggest that constitutively active CREB phosphorylation is important for the survival of mammalian cells in the brain.

References

Feb 1, 1995·Brain : a Journal of Neurology·O DevinskyB A Vogt
Apr 8, 1998·Annual Review of Neuroscience·A J SilvaS Kida
Jun 15, 1999·Trends in Biochemical Sciences·T R Soderling
Sep 27, 2001·Proceedings of the National Academy of Sciences of the United States of America·A E WestM E Greenberg
Apr 23, 2002·Nature Genetics·Theo MantamadiotisGünther Schütz
May 2, 2002·Trends in Cognitive Sciences·Glenn S. SandersChristoph Schmitz
May 2, 2002·Nature Medicine·Ted M Dawson, David D Ginty
May 15, 2002·Nature Neuroscience·Feng WeiMin Zhuo
Jul 10, 2003·Current Opinion in Neurobiology·Karl DeisserothRichard W Tsien
Jul 5, 2005·Nature Reviews. Neuroscience·Brent A Vogt

❮ Previous
Next ❯

Citations

Jun 23, 2010·Proceedings of the National Academy of Sciences of the United States of America·Nikolaos VolakakisThomas Perlmann
Dec 5, 2017·The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology·Tao JiangXue-Lian Du
Nov 4, 2010·Journal of Neurochemistry·Kensuke SakamotoKarl Obrietan
Feb 15, 2012·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·Theo MantamadiotisSebastian Dworkin

❮ Previous
Next ❯

Methods Mentioned

BETA
transfection

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis