Evidence map›Paper›PMID 31350900›Full record

ReviewNucleic acids research2019

DAXX in cancer: phenomena, processes, mechanisms and regulation.

Iqbal Mahmud, Daiqing Liao

Open access · goldAbstract readReview
In one paragraph

Review in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
10.4field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  6. Article
  7. Review
  8. Review
  9. NUSAP1 Recruits DAXX to Suppress HIF-Driven Triple-Negative Breast Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  18. Article
  19. Article
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Iqbal MahmudDepartment of Anatomy and Cell Biology, UF Health Cancer Center, University of Florida College of Medicine, 1333 Center Drive, Gainesville, FL 32610-0235, USA.
Daiqing LiaoDepartment of Anatomy and Cell Biology, UF Health Cancer Center, University of Florida College of Medicine, 1333 Center Drive, Gainesville, FL 32610-0235, USA.
University of Florida Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DAXX displays complex biological functions. Remarkably, DAXX overexpression is a common feature in diverse cancers, which correlates with tumorigenesis, disease progression and treatment resistance. Structurally, DAXX is modular with an N-terminal helical bundle, a docking site for many DAXX interactors (e.g. p53 and ATRX). DAXX's central region folds with the H3.3/H4 dimer, providing a H3.3-specific chaperoning function. DAXX has two functionally critical SUMO-interacting motifs. These modules are connected by disordered regions. DAXX's structural features provide a framework for deciphering how DAXX mechanistically imparts its functions and how its activity is regulated. DAXX modulates transcription through binding to transcription factors, epigenetic modifiers, and chromatin remodelers. DAXX's localization in the PML nuclear bodies also plays roles in transcriptional regulation. DAXX-regulated genes are likely important effectors of its biological functions. Deposition of H3.3 and its interactions with epigenetic modifiers are likely key events for DAXX to regulate transcription, DNA repair, and viral infection. Interactions between DAXX and its partners directly impact apoptosis and cell signaling. DAXX's activity is regulated by posttranslational modifications and ubiquitin-dependent degradation. Notably, the tumor suppressor SPOP promotes DAXX degradation in phase-separated droplets. We summarize here our current understanding of DAXX's complex functions with a focus on how it promotes oncogenesis.

Indexed as

Gene Expression Regulation, NeoplasticProtein Processing, Post-TranslationalAdaptor Proteins, Signal TransducingCell Line, TumorChromatinCo-Repressor ProteinsHumansMolecular ChaperonesNeoplasm ProteinsNeoplasmsNuclear ProteinsPhosphorylationProtein BindingProtein Interaction MappingSignal TransductionSumoylationAdaptor Proteins, Signal TransducingChromatinCo-Repressor ProteinsDAXX protein, humanMolecular ChaperonesNeoplasm ProteinsNuclear Proteins

Identifiers

PMID31350900
PMCPMC6735914
OpenAlexW2965027567

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.