Evidence map›Paper›PMID 26098514›Full record

ReviewAnnual review of biophysics2015

Regulation of Rad6/Rad18 Activity During DNA Damage Tolerance.

Mark Hedglin, Stephen J Benkovic

Abstract readReview
In one paragraph

Review in Annual review of biophysics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.0field-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

76 citing papers in PubMed, 117 citations in OpenAlex.

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16 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.

Mark HedglinDepartment of Chemistry, The Pennsylvania State University, University Park, Pennsylvania 16802; email: muh218@psu.edu , sjb1@psu.edu.
Stephen J Benkovic
Pennsylvania State University · US

Funding

Polymerase Switching During Translesion DNA Synthesis within the Human SystemF32CA165471 · NCI · PENNSYLVANIA STATE UNIVERSITY, THE · PI HEDGLIN, MARK · 2012 to 2014
$156k
NCI NIH HHS F32 CA165471NCI NIH HHS F32CA165471
6 · The paper itself

Abstract

Replicative polymerases (pols) cannot accommodate damaged template bases, and these pols stall when such offenses are encountered during S phase. Rather than repairing the damaged base, replication past it may proceed via one of two DNA damage tolerance (DDT) pathways, allowing replicative DNA synthesis to resume. In translesion DNA synthesis (TLS), a specialized TLS pol is recruited to catalyze stable, yet often erroneous, nucleotide incorporation opposite damaged template bases. In template switching, the newly synthesized sister strand is used as a damage-free template to synthesize past the lesion. In eukaryotes, both pathways are regulated by the conjugation of ubiquitin to the PCNA sliding clamp by distinct E2/E3 pairs. Whereas monoubiquitination by Rad6/Rad18 mediates TLS, extension of this ubiquitin to a polyubiquitin chain by Ubc13-Mms2/Rad5 routes DDT to the template switching pathway. In this review, we focus on the monoubiquitination of PCNA by Rad6/Rad18 and summarize the current knowledge of how this process is regulated.

Indexed as

DNA DamageDNA RepairDNA ReplicationAnimalsDNA-Binding ProteinsHumansProliferating Cell Nuclear AntigenUbiquitinUbiquitinationUbiquitin-Conjugating EnzymesDNA-Binding ProteinsProliferating Cell Nuclear AntigenUbiquitinUbiquitin-Conjugating EnzymesDNA damageDNA damage tolerancePCNARad6/Rad18ubiquitin

Identifiers

PMID26098514
PMCPMC5592839
OpenAlexW2152018334

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.