Send to

Choose Destination
Genesis. 2004 Oct;40(2):82-9.

Generation of a conditional allele of the CBP gene in mouse.

Author information

Molecular Genetics of Behavior, Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany.


CREB-binding protein (CBP) is an important transcriptional cofactor for various intracellular signaling pathways, including Ca(2+)- and cAMP-mediated gene activation. The loss of one CBP allele causes the human Rubinstein-Taybi syndrome, which is characterized by mental retardation and other severe developmental defects. Deletion of both CBP alleles in the mouse leads to early embryonic lethality. To address the function of CBP in late embryogenesis and in adult physiology, a floxed CBP allele (CBP(fl)) was generated. Using the Cre/loxP recombination system, CBP function was disrupted in principal forebrain neurons by breeding with a transgenic CaMKIIalpha-Cre mouse line to obtain CBP(fl/fl;CaMKIIalphaCre) mice. These mice contain CBP(stop523) alleles specifically in principal forebrain neurons, presumably resulting in the production of a truncated CBP protein unable to interact with a number of transcription factors, including phosphorylated CREB.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center