Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration.

By J. Alarcon, G. Malleret, K. Touzani, Svetlana Vronskaya, S. Ishii, E. Kandel, A. Barco. Neuron, 2004

933 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory (2019, background): “Knockdown or mutation of CBP impairs LTP and LTM (Alarcón et al. 2004; Korzus et al. 2004; Wood et al. 2005) and impairs LTF (Liu et al. 2013).”
Covalent modification of DNA regulates memory formation. (2007, neutral): “…structure serves as an important control mechanism in memory-associated transcriptional regulation (Swank and Sweatt, 2001; Guan et al., 2002; Huang et al., 2002; Levenson et al., 2004a, 2006; Korzus et al., 2004; Alarcon et al., 2004; Wood et al., 2005; Kumar et al., 2005; Chwang et al., 2006).”
Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation (2007, background): “HDAC inhibitors can ameliorate memory and LTP deficits in certain CBP mutant mice (Alarcon et al., 2004; Korzus et al., 2004).”