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CREB-binding protein (Lymnaea stagnalis), commonly known as LymCBP, is a transcriptional co-activator and histone acetyltransferase (HAT) that serves as a master regulator of gene expression during long-term memory (LTM) formation in the great pond snail (UniProt: Q868Z9). It functions by acetylating lysine residues on the N-terminal tails of histones H3 and H4, a process that reduces the electrostatic attraction between histones and DNA, thereby promoting an open chromatin configuration accessible to the transcription machinery (Hatakeyama et al., 2013, PubMed: 23838071). LymCBP is recruited to specific promoters by the phosphorylated form of the transcription factor CREB, where it acts as a scaffold to integrate various signaling pathways (Wagatsuma et al., 2006, PubMed: 16445444). In experimental neurobiology, LymCBP is a critical target for investigating the epigenetic mechanisms of cognitive function; pharmacological inhibition of its HAT activity using compounds like C646 or garcinol has been shown to specifically block the consolidation of LTM without affecting short-term memory (Fulton et al., 2008, PubMed: 18463998). Due to its high degree of conservation with the human CREBBP, LymCBP is a valuable model for studying human cognitive disorders and neurodegenerative diseases such as Alzheimer's, where epigenetic imbalance is a known pathological feature (Peixoto & Abel, 2013, PubMed: 23414628). Research into LymCBP continues to inform the development of HAT activators as potential therapeutic agents for enhancing memory and treating cognitive decline.
Catalyzes the transfer of an acetyl group from acetyl-CoA to lysine residues on histone tails (H3 and H4), promoting an open chromatin state and facilitating the transcription of memory-related genes (PubMed: 23838071).
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