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Science 15 July 1994:
Vol. 265. no. 5170, pp. 346 - 355
DOI: 10.1126/science.8023157
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Articles

Science, Vol 265, Issue 5170, 346-355
Copyright © 1994 by American Association for the Advancement of Science

articles

Crystal structure of a p53 tumor suppressor-DNA complex: understanding tumorigenic mutations

Y Cho, S Gorina, PD Jeffrey, and NP Pavletich

Cellular Biochemistry and Biophysics Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.

Mutations in the p53 tumor suppressor are the most frequently observed genetic alterations in human cancer. The majority of the mutations occur in the core domain which contains the sequence-specific DNA binding activity of the p53 protein (residues 102-292), and they result in loss of DNA binding. The crystal structure of a complex containing the core domain of human p53 and a DNA binding site has been determined at 2.2 angstroms resolution and refined to a crystallographic R factor of 20.5 percent. The core domain structure consists of a beta sandwich that serves as a scaffold for two large loops and a loop-sheet-helix motif. The two loops, which are held together in part by a tetrahedrally coordinated zinc atom, and the loop-sheet-helix motif form the DNA binding surface of p53. Residues from the loop-sheet-helix motif interact in the major groove of the DNA, while an arginine from one of the two large loops interacts in the minor groove. The loops and the loop-sheet-helix motif consist of the conserved regions of the core domain and contain the majority of the p53 mutations identified in tumors. The structure supports the hypothesis that DNA binding is critical for the biological activity of p53, and provides a framework for understanding how mutations inactivate it.


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C. Esser, M. Scheffner, and J. Hohfeld (2005)
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PDBSite: a database of the 3D structure of protein functional sites.
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M. Welin, U. Kosinska, N.-E. Mikkelsen, C. Carnrot, C. Zhu, L. Wang, S. Eriksson, B. Munch-Petersen, and H. Eklund (2004)
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L. Muller, A. Schaupp, D. Walerych, H. Wegele, and J. Buchner (2004)
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M. J. Demma, S. Wong, E. Maxwell, and B. Dasmahapatra (2004)
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J. Virol. 78, 10336-10347
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Nucleic Acids Res. 32, 2947-2956
   Abstract »    Full Text »    PDF »
Constitutive and DNA Damage Inducible Activation of pig3 and MDM2 Genes by Tumor-Derived p53 Mutant C277Y.
S. Pospisilova, C. Siligan, J. Ban, G. Jug, and H. Kovar (2004)
Mol. Cancer Res. 2, 296-304
   Abstract »    Full Text »    PDF »
How Many Mutant p53 Molecules Are Needed To Inactivate a Tetramer?.
W. M. Chan, W. Y. Siu, A. Lau, and R. Y. C. Poon (2004)
Mol. Cell. Biol. 24, 3536-3551
   Abstract »    Full Text »    PDF »
A global suppressor motif for p53 cancer mutants.
T. E. Baroni, T. Wang, H. Qian, L. R. Dearth, L. N. Truong, J. Zeng, A. E. Denes, S. W. Chen, and R. K. Brachmann (2004)
PNAS 101, 4930-4935
   Abstract »    Full Text »    PDF »
Association Between p53 Gene Mutations and Tobacco and Alcohol Exposure in Laryngeal Squamous Cell Carcinoma.
D. Ronchetti, C. B. Neglia, B. M. Cesana, N. Carboni, A. Neri, G. Pruneri, and L. Pignataro (2004)
Arch Otolaryngol Head Neck Surg 130, 303-306
   Abstract »    Full Text »    PDF »
Crystal Structure of a Superstable Mutant of Human p53 Core Domain: INSIGHTS INTO THE MECHANISM OF RESCUING ONCOGENIC MUTATIONS.
A. C. Joerger, M. D. Allen, and A. R. Fersht (2004)
J. Biol. Chem. 279, 1291-1296
   Abstract »    Full Text »    PDF »
Isolation of Temperature-sensitive p53 Mutations from a Comprehensive Missense Mutation Library.
K. Shiraishi, S. Kato, S.-Y. Han, W. Liu, K. Otsuka, M. Sakayori, T. Ishida, M. Takeda, R. Kanamaru, N. Ohuchi, et al. (2004)
J. Biol. Chem. 279, 348-355
   Abstract »    Full Text »    PDF »
Inhibition of mutant p53 expression and growth of DMS-153 small cell lung carcinoma by antagonists of growth hormone-releasing hormone and bombesin.
C. A. Kanashiro, A. V. Schally, K. Groot, P. Armatis, A. L. F. Bernardino, and J. L. Varga (2003)
PNAS 100, 15836-15841
   Abstract »    Full Text »    PDF »
TP53, BRCA1, and BRCA2 Tumor Suppressor Genes Are Not Commonly Mutated in Survivors of Hodgkin's Disease With Second Primary Neoplasms.
K. E. Nichols, J. A. Heath, D. Friedman, J. A. Biegel, A. Ganguly, P. Mauch, and L. Diller (2003)
J. Clin. Oncol. 21, 4505-4509
   Abstract »    Full Text »    PDF »
Prostate-Specific Expression of p53R172L Differentially Regulates p21, Bax, and mdm2 to Inhibit Prostate Cancer Progression and Prolong Survival.
I. Hernandez, L. A. Maddison, Y. Wei, F. DeMayo, T. Petras, B. Li, J. R. Gingrich, J. M. Rosen, and N. M. Greenberg (2003)
Mol. Cancer Res. 1, 1036-1047
   Abstract »    Full Text »    PDF »
Multiple Response Elements and Differential p53 Binding Control Perp Expression During Apoptosis.
E. E. Reczek, E. R. Flores, A. S. Tsay, L. D. Attardi, and T. Jacks (2003)
Mol. Cancer Res. 1, 1048-1057
   Abstract »    Full Text »    PDF »


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