ArticleFrontiers in genetics2013
Role of p97/VCP (Cdc48) in genome stability.
Article in Frontiers in genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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
55 citing papers in PubMed, 88 citations in OpenAlex.
- Induced degradation of Ufd1 reveals regulation of cohesin by the VCP/p97Life science alliance · 2026Article
- Cell-type-specific functionality encoded within the intrinsically disordered regions of OCT4.Nature communications · 2025Article
- Harnessing p97/VCP: A Transformative AAA+ ATPase Target for Next-Generation Cancer Therapeutics.Cancers · 2025Review
- Bacterial hitchhiking with drug-loaded nanoparticles as a drug delivery strategy for cancer immunotherapy.npj biomedical innovations · 2025Article
- Characterizing replisome disassembly in human cells.iScience · 2024Article
- Article
- p37 regulates VCP/p97 shuttling and functions in the nucleus and cytosol.Science advances · 2024Article
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Valosin-Containing Protein (VCP)/p97 Oligomerization.Sub-cellular biochemistry · 2024Review
- An autosomal-dominant childhood-onset disorder associated with pathogenic variants in VCP.American journal of human genetics · 2023Article
- Article
- TRAIP resolves DNA replication-transcription conflicts during the S-phase of unperturbed cells.Nature communications · 2023Article
- Ubx5-Cdc48 assists the protease Wss1 at DNA-protein crosslink sites in yeast.The EMBO journal · 2023Article
- Molecular Mechanisms Driving and Regulating the AAA+ ATPase VCP/p97, an Important Therapeutic Target for Treating Cancer, Neurological and Infectious Diseases.Biomolecules · 2023Review
- Cooperative assembly of p97 complexes involved in replication termination.Nature communications · 2022Article
- A Potential Mechanism for Targeting Aggregates With Proteasomes and Disaggregases in Liquid Droplets.Frontiers in aging neuroscience · 2022Review
- DNA Damage, Defective DNA Repair, and Neurodegeneration in Amyotrophic Lateral Sclerosis.Frontiers in aging neuroscience · 2022Review
- Phospho-SerCancers · 2021Article
- Coordinating DNA Replication and Mitosis through Ubiquitin/SUMO and CDK1.International journal of molecular sciences · 2021Review
- Targeting acute myeloid leukemia dependency on VCP-mediated DNA repair through a selective second-generation small-molecule inhibitor.Science translational medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ubiquitin-dependent molecular chaperone p97, also known as valosin-containing protein (VCP) or Cdc48, is an AAA ATPase involved in protein turnover and degradation. p97 converts its own ATPase hydrolysis into remodeling activity on a myriad of ubiquitinated substrates from different cellular locations and pathways. In this way, p97 mediates extraction of targeted protein from cellular compartments or protein complexes. p97-dependent protein extraction from various cellular environments maintains cellular protein homeostasis. In recent years, p97-dependent protein extraction from chromatin has emerged as an essential evolutionarily conserved process for maintaining genome stability. Inactivation of p97 segregase activity leads to accumulation of ubiquitinated substrates on chromatin, consequently leading to protein-induced chromatin stress (PICHROS). PICHROS directly and negatively affects multiple DNA metabolic processes, including replication, damage responses, mitosis, and transcription, leading to genotoxic stress and genome instability. By summarizing and critically evaluating recent data on p97 function in various chromatin-associated protein degradation processes, we propose establishing p97 as a genome caretaker.
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.