Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Robust p53 Stabilization Is Dispensable for Its Activation and Tumor Suppressor Function.

Cancer research - 15 Feb 2021

Kon Ning, Churchill Michael, Li Huan, Mukherjee Siddhartha, Manfredi James J, Gu Wei

Abstract excerpt

p53 is a short-lived protein with low basal levels under normal homeostasis conditions. However, upon DNA damage, levels of p53 dramatically increase for its activation. Although robust stabilization of p53 serves as a "trademark" for DNA damage responses, the requirement for such dramatic protein stabilization in tumor suppression has not been well addressed. Here we generated a mutant p53KQ mouse where all the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acetylation
Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genes, Tumor Suppressor

Share to Lysine

Share to Mutant Proteins

Share to Pancreatic Neoplasms

Share to Protein Processing, Post-Translational

Share to Protein Stability

Source

Open in PubMed Open full text

Identifiers

PMID: 33323382
DOI: 10.1158/0008-5472.CAN-20-1804
PMCID: PMC8026563

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Robust p53 Stabilization Is Dispensable for Its Activation and Tumor Suppressor Function.PMID 33323382Read ↗

The role of acetylation sites in the regulation of p53 activity.Semantic proximity Read ↗

mTOR inhibition acts as an unexpected checkpoint in p53-mediated tumor suppression.Semantic proximity Read ↗

Acetylation Is Crucial for p53-Mediated Ferroptosis and Tumor Suppression.Semantic proximity Read ↗

Full p53 transcriptional activation potential is dispensable for tumor suppression in diverse lineages.Semantic proximity Read ↗

The C terminus of p53 regulates gene expression by multiple mechanisms in a target- and tissue-specific manner in vivo.Semantic proximity Read ↗

Tumor suppression in the absence of p53-mediated cell-cycle arrest, apoptosis, and senescence.Semantic proximity Read ↗

The C-terminal lysines fine-tune P53 stress responses in a mouse model but are not required for stability control or transactivation.Semantic proximity Read ↗

Drug-Induced p53 Activation Limits Pancreatic Cancer InitiationSemantic proximity Read ↗

Insights into the limitations of transient expression systems for the functional study of p53 acetylation site and oncogenic mutants.Semantic proximity Read ↗

Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression.Semantic proximity Read ↗

Loss of peptidase D binding restores the tumor suppressor functions of oncogenic p53 mutants.Semantic proximity Read ↗

p53 Activation in Genetic Disorders: Different Routes to the Same Destination.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.