Evidence map›Paper›PMID 29871913›Full record

ArticleScience signaling2018

K63-linked polyubiquitin chains bind to DNA to facilitate DNA damage repair.

Pengda Liu, Wenjian Gan, Siyuan Su, Arthur V Hauenstein, Tian-Min Fu, Bradley Brasher, Carsten Schwerdtfeger, Anthony C Liang, Ming Xu, Wenyi Wei

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  10. Covalent inhibition ofiScience · 2025
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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

10 authors at 5 institutions in 1 country.

Pengda LiuDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. pengda_liu@med.unc.edu wwei2@bidmc.harvard.edu.ORCID 0000-0003-2755-3601
Wenjian GanDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Siyuan SuDepartment of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Arthur V HauensteinDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA.
Tian-Min FuDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA.ORCID 0000-0002-6281-1752
Bradley BrasherBoston Biochem Inc., Cambridge, MA 02139, USA.
Carsten SchwerdtfegerBoston Biochem Inc., Cambridge, MA 02139, USA.
Anthony C LiangDepartment of Genetics and Howard Hughes Medical Institute, Division of Genetics, Brigham and Women's Hospital, Harvard University Medical School, Boston, MA 02115, USA.
Ming XuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. pengda_liu@med.unc.edu wwei2@bidmc.harvard.edu.ORCID 0000-0003-0512-3811
Beth Israel Deaconess Medical Center · USBiogen (United States) · USBoston Children's Hospital · USHoward Hughes Medical Institute · USUniversity of North Carolina at Chapel Hill · US

Funding

Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
Functional analysis of beta-TRCP in cell cycle control and DNA damage responseR01GM094777 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2012 to 2015
$1.3M
Elucidating a Novel Akt Activation Mechanism for Targeted Prostate Cancer TherapyR00CA181342 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, PENGDA · 2016 to 2018
$653k
Elucidating a Novel Akt Activation Mechanism for Targeted Prostate Cancer TherapyK99CA181342 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LIU, PENGDA · 2014 to 2015
$339k
Elucidating Novel Akt Regulatory Mechanisms to Overcome Akt-mediated Therapeutic Resistance in Breast CancerK99CA207867 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GAN, WENJIAN · 2016 to 2017
$338k
NCI NIH HHS K99 CA181342NCI NIH HHS K99 CA207867NCI NIH HHS R00 CA181342NCI NIH HHS R01 CA177910NIGMS NIH HHS R01 GM094777
6 · The paper itself

Abstract

Polyubiquitylation is canonically viewed as a posttranslational modification that governs protein stability or protein-protein interactions, in which distinct polyubiquitin linkages ultimately determine the fate of modified protein(s). We explored whether polyubiquitin chains have any nonprotein-related function. Using in vitro pull-down assays with synthetic materials, we found that polyubiquitin chains with the Lys

Indexed as

DNA DamageDNA RepairDNAHumansLysineModels, MolecularNeoplasmsPolyubiquitinProtein Processing, Post-TranslationalSignal TransductionTumor Cells, CulturedUbiquitinationDNALysinePolyubiquitin

Identifiers

PMID29871913
PMCPMC6434707
OpenAlexW2807341565

What OpenQuestion holds

Textmetadata
LicenceTDM
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.