Evidence map›Paper›PMID 37096048›Full record

ArticleiScience2023

DTX3L E3 ligase targets p53 for degradation at poly ADP-ribose polymerase-associated DNA damage sites.

Qingsheng Yan, Jingyi Ding, Sumbul Jawed Khan, Lee N Lawton, Margaret A Shipp

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  12. PARP9-PARP13-PARP14 axis tunes colorectal cancer response to radiotherapy.Journal of experimental & clinical cancer research : CR · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Qingsheng YanDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Jingyi DingDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Sumbul Jawed KhanDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Lee N LawtonDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Margaret A ShippDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Dana-Farber Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P53 is a master transcriptional regulator and effector of the DNA damage response (DDR) that localizes to DNA damage sites, in part, via an interaction with PARP1. However, the mechanisms that regulate p53 abundance and activity at PARP1-decorated DNA damage sites remain undefined. The PARP9 (BAL1) macrodomain-containing protein and its partner DTX3L (BBAP) E3 ligase are rapidly recruited to PARP1-PARylated DNA damage sites. During an initial DDR, we found that DTX3L rapidly colocalized with p53, polyubiquitylated its lysine-rich C-terminal domain, and targeted p53 for proteasomal degradation. DTX3L knockout significantly increased and prolonged p53 retention at PARP-decorated DNA damage sites. These findings reveal a non-redundant, PARP- and PARylation-dependent role for DTX3L in the spatiotemporal regulation of p53 during an initial DDR. Our studies suggest that targeted inhibition of DTX3L may augment the efficacy of certain DNA-damaging agents by increasing p53 abundance and activity.

Indexed as

Biochemical mechanismCell biologyMolecular mechanism of gene regulation

Identifiers

PMID37096048
PMCPMC10122052
OpenAlexW4327703883

What OpenQuestion holds

Textmetadata
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.