The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: implications for a dominant-negative mechanism
Abstract
A mouse model of Rubinstein-Taybi syndrome (RTS) was generated by an insertional mutation into the cyclic AMP response element-binding protein (CREB)-binding protein (CBP) gene. Heterozygous CBP-deficient mice, which had truncated CBP protein (residues 1-1084) containing the CREB-binding domain (residues 462-661), showed clinical features of RTS, such as growth retardation (100%), retarded osseous maturation (100%), hypoplastic maxilla with narrow palate (100%), cardiac anomalies (15%) and skeletal abnormalities (7%). Truncated CBP is considered to have been acting during development as a dominant-negative inhibitor to lead to the phenotypes of RTS in mice. Our studies with step-through-type passive avoidance tests and with fear conditioning test showed that mice were deficient in long-term memory (LTM). In contrast, short-term memory (STM) appeared to be normal. These results implicate a crucial role for CBP in mammalian LTM. Our CBP +/- mice would be an excellent model for the study of the role of CBP in development and memory storage mechanisms.
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Phosphorylated CREB binds specifically to the nuclear protein CBP
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Nuclear protein CBP is a coactivator for the transcription factor CREB
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Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP
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Role of CBP/P300 in nuclear receptor signalling
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Cited by
The coregulator exchange in transcriptional functions of nuclear receptors
Glass, C. K., & Rosenfeld, M. G. (2000) · Genes & Development · doi:10.1101/gad.14.2.121 · Cited by 2,233
CBP/p300 in cell growth, transformation, and development
Goodman, R. H., & Smolik, S. (2000) · Genes & Development · doi:10.1101/gad.14.13.1553 · Cited by 1,778
Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials
Cheng, Y., He, C., Wang, M., Ma, X., Mo, F., Yang, S., Han, J., & Wei, X. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0095-0 · Cited by 1,097
“Knockout of CBP/p300 is lethal for early embryonic mouse models.(171,172) The acetyl group transfer strategies for each HAT subfamily are different.”
BackgroundPape, H.-C., & Pare, D. (2010) · Physiological Reviews · doi:10.1152/physrev.00037.2009 · Cited by 994
Rosenfeld, M. G., Lunyak, V. V., & Glass, C. K. (2006) · Genes & Development · doi:10.1101/gad.1424806 · Cited by 952
Metadata
- Authors
- Oike, Y.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-03-01
- Volume
- 8
- Issue
- 3
- Pages
- 387-396
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2106193559
- Cited by
- 305
- References
- 39
- FWCI
- 11.85
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: implications for a dominant-negative mechanism. https://app.cochat.ai/papers/10.1093/hmg/8.3.387
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- Oike, Y. (1999). Truncated CBP protein leads to classical Rubinstein-Taybi syndrome phenotypes in mice: implications for a dominant-negative mechanism. Human Molecular Genetics. https://doi.org/10.1093/hmg/8.3.387
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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