Evidence map›Paper›PMID 27906959›Full record

ArticlePLoS genetics2016

PCNA-Dependent Cleavage and Degradation of SDE2 Regulates Response to Replication Stress.

Ukhyun Jo, Winson Cai, Jingming Wang, Yoojin Kwon, Alan D D'Andrea, Hyungjin Kim

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  4. Biology · 2025
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  13. Signaling Pathways Regulated by UBR Box-Containing E3 Ligases.International journal of molecular sciences · 2021
    Review
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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

6 authors at 2 institutions in 1 country.

Ukhyun JoDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, New York, United States of America.
Winson CaiDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, New York, United States of America.
Jingming WangDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, New York, United States of America.
Yoojin KwonDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, New York, United States of America.
Alan D D'AndreaDepartment of Radiation Oncology and Center for DNA damage and Repair, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
Hyungjin KimDepartment of Pharmacological Sciences, Stony Brook University, Stony Brook, New York, United States of America.ORCID http://orcid.org/0000-0003-1913-6373
Stony Brook University · USDana-Farber Cancer Institute · US

Funding

MOLECULAR PATHOGENESIS OF FANCONI ANEMIAR01HL052725 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI ALAN D. D'ANDREA · 1994 to 2026
$5.9M
NHLBI NIH HHS R01 HL052725
6 · The paper itself

Abstract

Maintaining genomic integrity during DNA replication is essential for cellular survival and for preventing tumorigenesis. Proliferating cell nuclear antigen (PCNA) functions as a processivity factor for DNA replication, and posttranslational modification of PCNA plays a key role in coordinating DNA repair against replication-blocking lesions by providing a platform to recruit factors required for DNA repair and cell cycle control. Here, we identify human SDE2 as a new genome surveillance factor regulated by PCNA interaction. SDE2 contains an N-terminal ubiquitin-like (UBL) fold, which is cleaved at a diglycine motif via a PCNA-interacting peptide (PIP) box and deubiquitinating enzyme activity. The cleaved SDE2 is required for negatively regulating ultraviolet damage-inducible PCNA monoubiquitination and counteracting replication stress. The cleaved SDE2 products need to be degraded by the CRL4CDT2 ubiquitin E3 ligase in a cell cycle- and DNA damage-dependent manner, and failure to degrade SDE2 impairs S phase progression and cellular survival. Collectively, this study uncovers a new role for CRL4CDT2 in protecting genomic integrity against replication stress via regulated proteolysis of PCNA-associated SDE2 and provides insights into how an integrated UBL domain within linear polypeptide sequence controls protein stability and function.

Indexed as

CarcinogenesisChemokine CXCL12DNA-Binding ProteinsDNA DamageDNA RepairDNA ReplicationHeLa CellsHumansProliferating Cell Nuclear AntigenProtein StabilityProteolysisReceptors, Interleukin-17S PhaseUbiquitinationUbiquitin-Protein LigasesUltraviolet RaysChemokine CXCL12CXCL12 protein, humanDNA-Binding ProteinsIL17RB protein, humanProliferating Cell Nuclear AntigenReceptors, Interleukin-17SDE2 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID27906959
PMCPMC5131917
OpenAlexW2559242301

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.