The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
The CREB/CRE transcriptional pathway: protection against oxidative stress‐mediated neuronal cell death
Open accessAbstract
Formation of reactive oxygen and nitrogen species is a precipitating event in an array of neuropathological conditions. In response to excessive reactive oxygen species (ROS) levels, transcriptionally dependent mechanisms drive the up‐regulation of ROS scavenging proteins which, in turn, limit the extent of brain damage. Here, we employed a transgenic approach in which cAMP‐response element binding protein (CREB)‐mediated transcription is repressed (via A‐CREB) to examine the contribution of the CREB/cAMP response element pathway to neuroprotection and its potential role in limiting ROS toxicity. Using the pilocarpine‐evoked repetitive seizure model, we detected a marked enhancement of cell death in A‐CREB transgenic mice. Paralleling this, there was a dramatic increase in tyrosine nitration (a marker of reactive species formation) in A‐CREB transgenic mice. In addition, inducible expression of peroxisome proliferator‐activated receptor gamma coactivator‐1α was diminished in A‐CREB transgenic mice, as was activity of complex I of the mitochondrial electron transport chain. Finally, the neuroprotective effect of brain‐derived neurotrophic factor (BDNF) against ROS‐mediated cell death was abrogated by disruption of CREB‐mediated transcription. Together, these data both extend our understanding of CREB functionality and provide in vivo validation for a model in which CREB functions as a pivotal upstream integrator of neuroprotective signaling against ROS‐mediated cell death.
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Cites
Oxidative stress and neurodegeneration: where are we now?
Halliwell, B. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03907.x · Cited by 2,614
St-Pierre, J., Drori, S., Uldry, M., Silvaggi, J. M., Rhee, J., Jäger, S., Handschin, C., Zheng, K., Lin, J., Yang, W., et al. (2006) · Cell · doi:10.1016/j.cell.2006.09.024 · Cited by 2,233
Function and regulation of CREB family transcription factors in the nervous system
Lonze, B. E., & Ginty, D. D. (2002) · Neuron · doi:10.1016/s0896-6273(02)00828-0 · Cited by 2,127
Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways
Hardingham, G. E., Fukunaga, Y., & Bading, H. (2002) · Nature Neuroscience · doi:10.1038/nn835 · Cited by 1,686
Control of memory formation through regulated expression of a CaMKII transgene
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Disruption of CREB function in brain leads to neurodegeneration
Mantamadiotis, T., Lemberger, T., Bleckmann, S. C., Kern, H., Kretz, O., Villalba, A. M., Tronche, F., Kellendonk, C., Gau, D., Kapfhammer, J., et al. (2002) · Nature Genetics · doi:10.1038/ng882 · Cited by 684
Perluigi, M., Joshi, G., Sultana, R., Calabrese, V., De Marco, C., Coccia, R., Cini, C., & Butterfield, D. A. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20879 · Cited by 125 · cited 2×
“Importantly, in animal disease models, pharmacological approaches designed to reduce the oxidative load afford significant neuroprotection (Crow et al. 2005; Perluigi et al. 2006; Liang et al. 2007), thus attesting to the critical role that oxidative stress plays in a diverse array of neurological diseases and disorde…”
BackgroundBedogni, B., Pani, G., Colavitti, R., Riccio, A., Borrello, S., Murphy, M., Smith, R., Eboli, M. L., & Galeotti, T. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m301089200 · Cited by 124
Cited by
Sakamoto, K., Karelina, K., & Obrietan, K. (2011) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2010.07080.x · Cited by 543
Self-citationVisualising associations between paired ‘omics’ data sets
González, I., Cao, K.-A. L., Davis, M. J., & Déjean, S. (2012) · BioData Mining · doi:10.1186/1756-0381-5-19 · Cited by 313
Benoit, M. E., Hernandez, M. X., Dinh, M. L., Benavente, F., Vasquez, O., & Tenner, A. J. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.400168 · Cited by 155
NR4A orphan nuclear receptors as mediators of CREB-dependent neuroprotection
Volakakis, N., Kadkhodaei, B., Joodmardi, E., Wallis, K., Panman, L., Silvaggi, J., Spiegelman, B. M., & Perlmann, T. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1007088107 · Cited by 167
A model of the mitochondrial basis of bipolar disorder
Morris, G., Walder, K., McGee, S. L., Dean, O. M., Tye, S. J., Maes, M., & Berk, M. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.01.014 · Cited by 162
Metadata
- Authors
- Lee, B., Cao, R., Choi, Y., Cho, H., Rhee, A. D., Hah, C. K., Hoyt, K. R., & Obrietan, K.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2009-02-09
- Volume
- 108
- Issue
- 5
- Pages
- 1251-1265
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1982012586
- Cited by
- 167
- References
- 8
- FWCI
- 2.73
- Type
- journal article
- Language
- en
- Open access
- green
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- Lee, B., Cao, R., Choi, Y., Cho, H., Rhee, A. D., Hah, C. K., Hoyt, K. R., & Obrietan, K. (2009). The CREB/CRE transcriptional pathway: protection against oxidative stress‐mediated neuronal cell death. Journal of Neurochemistry. https://doi.org/10.1111/j.1471-4159.2008.05864.x
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