Mouse mutants reveal that putative protein interaction sites in the p53 proline-rich domain are dispensable for tumor suppression. [electronic resource]
Producer: 20070316Description: 1425-32 p. digitalISSN:- 0270-7306
- Amino Acid Sequence
- Animals
- Apoptosis
- Binding Sites
- Cell Cycle
- Cell Proliferation
- Cell Transformation, Neoplastic
- Conserved Sequence
- DNA Damage
- Fibroblasts -- cytology
- Gene Targeting
- Mice
- Mice, Mutant Strains
- Molecular Sequence Data
- Mutant Proteins -- metabolism
- Neoplasms -- pathology
- Point Mutation -- genetics
- Proline -- metabolism
- Protein Binding
- Protein Structure, Tertiary
- Recombination, Genetic -- genetics
- Structure-Activity Relationship
- Transcriptional Activation -- genetics
- Tumor Suppressor Protein p53 -- chemistry
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Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
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