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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kung, A. L. Rebel, V. I. Bronson, R. T. Ch'ng, L. E. Sieff, C. A. Livingston, D. M. Yao, T. P. |
| Description | Country affiliation: United States Author Affiliation: Kung AL ( Dana-Farber Cancer Institute, and Harvard Medical School, Boston, Massachusetts 02115, USA.) |
| Abstract | Mice with monoallelic inactivation of the CBP gene develop highly penetrant, multilineage defects in hematopoietic differentiation and, with advancing age, an increased incidence of hematologic malignancies. The latter are characterized, at least in some cases, by loss of heterozygosity (LOH) at the CBP locus. No such pathology was observed in wild-type or p300 heterozygous null mice of the same age and genetic background. Thus, a full complement of CBP, but not p300, is required for normal hematopoietic differentiation. These results also provide the first experimental evidence for the hypothesis that CBP has tumor-suppressing activity. |
| File Format | HTM / HTML |
| ISSN | 08909369 |
| e-ISSN | 15495477 |
| Journal | Genes & Development |
| Issue Number | 3 |
| Volume Number | 14 |
| Language | English |
| Publisher | Cold Spring Harbor Laboratory Press |
| Publisher Date | 2000-02-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Molecular Discipline Biology__semicolon__developmental Discipline Biology__semicolon__genetics__semicolon__cell Discipline Biology Genes, Tumor Suppressor Genetics Hematologic Neoplasms Hematopoiesis Nuclear Proteins Trans-activators Animals Blotting, Southern Blotting, Western Bone Marrow Transplantation Creb-binding Protein Cell Transplantation E1a-associated P300 Protein Pathology Heterozygote Loss Of Heterozygosity Mice Mice, Inbred C57bl Mice, Knockout Metabolism Phenotype Spleen Cytology Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, P.h.s. |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Developmental Biology |
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