ReviewCold Spring Harbor perspectives in biology2010
The tumor suppressor p53: from structures to drug discovery.
Review in Cold Spring Harbor perspectives in biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
193 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Article
- DeepPNI: a language- and graph-based model for mutation-driven protein-nucleic acid binding energetics.Nucleic acids research · 2026Article
- Bispecific Antibodies for Acute Myeloid Leukemia: From Bone Marrow Immune Niche to Clinical Translation.Antibodies (Basel, Switzerland) · 2026Review
- SPPIDER-seq: sequence-based partner-aware predictor of protein-protein interaction sites.Bioinformatics (Oxford, England) · 2026Article
- A zero-parameter first-principles gate framework for full-length TP53 missense variant interpretation.PLoS computational biology · 2026Article
- Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding.bioRxiv : the preprint server for biology · 2026Article
- SPPIDER-seq: Sequence-based partner-aware predictor of protein-protein interaction sites.bioRxiv : the preprint server for biology · 2026Article
- Shared gene signatures and biochemical regulatory networks linking Parkinson's disease and ulcerative colitis.NPJ Parkinson's disease · 2026Article
- A catalogue of missense and nonsense mutation abundances for the U.S. cancer patient population.medRxiv : the preprint server for health sciences · 2026Article
- GenReP: An Ensemble Model for Predicting TP53 in Response to Pharmaceutical Compounds.Molecules (Basel, Switzerland) · 2026Article
- Lung cancer-enriched p53 mutants occupy canonical p53 target genes without activating transcription, revealing a distinct loss-of-function behavior.bioRxiv : the preprint server for biology · 2026Article
- Synergistic antitumor effect of oroxylin A and donafenib in hepatocellular carcinoma through tumor protein p53 signaling pathway activation.World journal of gastroenterology · 2026Article
- Characterization of the Second-Generation Covalent Fragment Library (CovLib Gen2): Thiol Reactivity Profiling and p53-Y220C Rescue.Drug design, development and therapy · 2026Article
- Biology of PEST-containing nuclear proteins as potential targets in ovarian cancer (Review).Oncology letters · 2026Review
- TowardsbioRxiv : the preprint server for biology · 2025Article
- Hallmarks and mechanisms of cellular senescence in aging and disease.Cell death discovery · 2025Review
- Transcription Factors and Methods for the Pharmacological Correction of Their Activity.International journal of molecular sciences · 2025Review
- The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- TP53-Mutated Acute Myeloid Leukemia: Unanswered Questions.Hematological oncology · 2025Review
133 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Even 30 years after its discovery, the tumor suppressor protein p53 is still somewhat of an enigma. p53's intimate and multifaceted role in the cell cycle is mirrored in its equally complex structural biology that is being unraveled only slowly. Here, we discuss key structural aspects of p53 function and its inactivation by oncogenic mutations. Concerted action of folded and intrinsically disordered domains of the highly dynamic p53 protein provides binding promiscuity and specificity, allowing p53 to process a myriad of cellular signals to maintain the integrity of the human genome. Importantly, progress in elucidating the structural biology of p53 and its partner proteins has opened various avenues for structure-guided rescue of p53 function in tumors. These emerging anticancer strategies include targeting mutant-specific lesions on the surface of destabilized cancer mutants with small molecules and selective inhibition of p53's degradative pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.