The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Abnormal skeletal patterning in embryos lacking a single Cbp allele: A partial similarity with Rubinstein–Taybi syndrome
Open accessAbstract
CBP is a transcriptional coactivator required by many transcription factors for transactivation. Rubinstein–Taybi syndrome, which is an autosomal dominant syndrome characterized by abnormal pattern formation, has been shown to be associated with mutations in the Cbp gene. Furthermore, Drosophila CBP is required in hedgehog signaling for the expression of decapentapleigic , the Drosophila homologue of bone morphogenetic protein. However, no direct evidence exists to indicate that loss of one copy of the mammalian Cbp gene affects pattern formation. Here, we show that various abnormalities occur at high frequency in the skeletal system of heterozygous Cbp -deficient mice resulting from a C57BL/6-CBA × BALB/c cross. In support of a conserved signaling pathway for pattern formation in insects and mammals, the expression of Bmp7 was found to be reduced in the heterozygous mutants. The frequency of the different abnormalities was significantly lower in a C57BL/6-CBA background, suggesting that the genetic background is an important determinant of the variability and severity of the anomalies seen in Rubinstein–Taybi syndrome patients.
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Cites
Phosphorylated CREB binds specifically to the nuclear protein CBP
Chrivia, J. C., Kwok, R. P. S., Lamb, N., Hagiwara, M., Montminy, M. R., & Goodman, R. H. (1993) · Nature · doi:10.1038/365855a0 · Cited by 2,052
Bourtchuladze, R., Frenguelli, B., Blendy, J., Cioffi, D., Schutz, G., & Silva, A. J. (1994) · Cell · doi:10.1016/0092-8674(94)90400-6 · Cited by 1,800
Nuclear protein CBP is a coactivator for the transcription factor CREB
Kwok, R. P. S., Lundblad, J. R., Chrivia, J. C., Richards, J. P., Bächinger, H. P., Brennan, R. G., Roberts, S. G. E., Green, M. R., & Goodman, R. H. (1994) · Nature · doi:10.1038/370223a0 · Cited by 1,443
Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP
Petrif, F., Giles, R. H., Dauwerse, H. G., Saris, J. J., Hennekam, R. C. M., Masuno, M., Tommerup, N., van Ommen, G.-J. B., Goodman, R. H., Peters, D. J. M., et al. (1995) · Nature · doi:10.1038/376348a0 · Cited by 1,217
A family of transcriptional adaptor proteins targeted by the E1A oncoprotein
Arany, Z., Newsome, D., Oldread, E., Livingston, D. M., & Eckner, R. (1995) · Nature · doi:10.1038/374081a0 · Cited by 533
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
p300/CBP proteins: HATs for transcriptional bridges and scaffolds
Chan, H. M., & La Thangue, N. B. (2001) · Journal of Cell Science · doi:10.1242/jcs.114.13.2363 · Cited by 1,092
Coregulator Function: A Key to Understanding Tissue Specificity of Selective Receptor Modulators
Smith, C. L., & O’Malley, B. W. (2004) · Endocrine Reviews · doi:10.1210/er.2003-0023 · Cited by 931
Chromatin Acetylation, Memory, and LTP Are Impaired in CBP+/− Mice
Alarcón, J. M., Malleret, G., Touzani, K., Vronskaya, S., Ishii, S., Kandel, E. R., & Barco, A. (2004) · Neuron · doi:10.1016/j.neuron.2004.05.021 · Cited by 892
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Metadata
- Authors
- Tanaka, Y., Naruse, I., Maekawa, T., Masuya, H., Shiroishi, T., & Ishii, S.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1997-09-16
- Volume
- 94
- Issue
- 19
- Pages
- 10215-10220
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1975580948
- Cited by
- 294
- References
- 5
- FWCI
- 14.26
- Type
- journal article
- Language
- en
- Open access
- green
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- Tanaka, Y., Naruse, I., Maekawa, T., Masuya, H., Shiroishi, T., & Ishii, S. (1997). Abnormal skeletal patterning in embryos lacking a single Cbp allele: A partial similarity with Rubinstein–Taybi syndrome. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.94.19.10215
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