Evidence map›Paper›PMID 33753087›Full record

ReviewProgress in biophysics and molecular biology2021

DNA glycosylase NEIL2 functions in multiple cellular processes.

Altaf H Sarker, Priscilla K Cooper, Tapas K Hazra

Open access · greenAbstract readReview
In one paragraph

Review in Progress in biophysics and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
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

3 authors at 2 institutions in 1 country.

Altaf H SarkerBiological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA, 94720, USA. Electronic address: AHSarker@lbl.gov.
Priscilla K CooperBiological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA, 94720, USA.
Tapas K HazraUniversity of Texas Medical Branch, Galveston, TX, 77555, USA.
Lawrence Berkeley National Laboratory · USThe University of Texas Medical Branch at Galveston · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI WALTER J. CHAZIN · 2001 to 2026
$89.6M
Role of Cytosolic DNA-multiprotein Interactome in Allergic Airway InflammationR01HL145477 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HAZRA, TAPAS K, SUR, SANJIV · 2019 to 2022
$3.6M
Preferential single-strand break repair in the active genes of mammalian cellsR01NS073976 · NINDS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HAZRA, TAPAS K · 2012 to 2021
$3.3M
NCI NIH HHS P01 CA092584NHLBI NIH HHS R01 HL145477NINDS NIH HHS R01 NS073976
6 · The paper itself

Abstract

Cell survival largely depends on the faithful maintenance of genetic material since genomic DNA is constantly exposed to genotoxicants from both endogenous and exogenous sources. The evolutionarily conserved base excision repair (BER) pathway is critical for maintaining genome integrity by eliminating highly abundant and potentially mutagenic oxidized DNA base lesions. BER is a multistep process, which is initiated with recognition and excision of the DNA base lesion by a DNA glycosylase, followed by DNA end processing, gap filling and finally sealing of the nick. Besides genome maintenance by global BER, DNA glycosylases have been found to play additional roles, including preferential repair of oxidized lesions from transcribed genes, modulation of the immune response, participation in active DNA demethylation and maintenance of the mitochondrial genome. Central to these functions is the DNA glycosylase NEIL2. Its loss results in increased accumulation of oxidized base lesions in the transcribed genome, triggers an immune response and causes early neurodevelopmental defects, thus emphasizing the multitasking capabilities of this repair protein. Here we review the specialized functions of NEIL2 and discuss the consequences of its absence both in vitro and in vivo.

Indexed as

DNA GlycosylasesAnimalsDNADNA-(Apurinic or Apyrimidinic Site) LyaseDNA DamageDNA RepairHumansDNADNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesBERCancerDemethylationDNA glycosylase NEIL2InflammationTC-BER

Identifiers

PMID33753087
PMCPMC10277195
OpenAlexW3138977751

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.