Because of its association with CBP, understanding the role of CBP in neurological pathways and how aberrations influence disease is becoming of increasing interest. Numerous animal models have been designed in order to evaluate changes in motor, learning and memory function in mice with CBP mutations. Conditional knockout (cKO) mice that were hemizygous for CBP or had CBP point mutations exhibited memory defects—specifically related to long-term memory. For mice with homozygous point mutations in their CBP KIX domain, they demonstrated impaired motor skill learning and execution. In conjunction with the neurological challenges experienced by RTS (Rubinstein–Taybi syndrome) patients (lower levels of intelligence, attention deficits), CBP is attributable to a variety of neurological symptoms characteristic of many different types of diseases.

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