Evidence map›Paper›PMID 26460502›Full record

ArticleThe FEBS journal2016

Inhibition of APOBEC3G activity impedes double-stranded DNA repair.

Ponnandy Prabhu, Shivender M D Shandilya, Elena Britan-Rosich, Adi Nagler, Celia A Schiffer, Moshe Kotler

Open access · bronzeAbstract read
In one paragraph

Article in The FEBS journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Genome instability and lymphoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  8. Article
  9. APOBEC3s: DNA-editing human cytidine deaminases.Protein science : a publication of the Protein Society · 2019
    Review
  10. Review
  11. Article
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 3 institutions in 2 countries.

Ponnandy PrabhuDepartment of Pathology and Immunology, the Lautenberg Center for General and Tumor Immunology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Shivender M D ShandilyaDepartment of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA, USA.
Elena Britan-RosichDepartment of Pathology and Immunology, the Lautenberg Center for General and Tumor Immunology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Adi NaglerDepartment of Pathology and Immunology, the Lautenberg Center for General and Tumor Immunology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Celia A SchifferDepartment of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA, USA.
Moshe KotlerDepartment of Pathology and Immunology, the Lautenberg Center for General and Tumor Immunology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Concern Foundation · USUniversity of Massachusetts Chan Medical School · USHebrew University of Jerusalem · IL

Funding

Structural Characterization of APOBECS's Atomic interactionsP01GM091743 · NIGMS · UNIVERSITY OF MINNESOTA · PI KOTLER, MOSHE · 2011 to 2015
$10.1M
Structurally dissecting APOBEC3's for HIV-1 restrictionR01GM118474 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SCHIFFER, CELIA A. · 2016 to 2018
$1.8M
NIGMS NIH HHS P01 GM091743NIGMS NIH HHS R01 GM118474
6 · The paper itself

Abstract

The cellular cytidine deaminase APOBEC3G (A3G) was first described as an anti-HIV-1 restriction factor, acting by directly deaminating reverse transcripts of the viral genome. HIV-1 Vif neutralizes the activity of A3G, primarily by mediating degradation of A3G to establish effective infection in host target cells. Lymphoma cells, which express high amounts of A3G, can restrict Vif-deficient HIV-1. Interestingly, these cells are more stable in the face of treatments that result in double-stranded DNA damage, such as ionizing radiation and chemotherapies. Previously, we showed that the Vif-derived peptide (Vif25-39) efficiently inhibits A3G deamination, and increases the sensitivity of lymphoma cells to ionizing radiation. In the current study, we show that additional peptides derived from Vif, A3G, and APOBEC3F, which contain the LYYF motif, inhibit deamination activity. Each residue in the Vif25-39 sequence moderately contributes to the inhibitory effect, whereas replacing a single residue in the LYYF motif completely abrogates inhibition of deamination. Treatment of A3G-expressing lymphoma cells exposed to ionizing radiation with the new inhibitory peptides reduces double-strand break repair after irradiation. Incubation of cultured irradiated lymphoma cells with peptides that inhibit double-strand break repair halts their propagation. These results suggest that A3G may be a potential therapeutic target that is amenable to peptide and peptidomimetic inhibition.

Indexed as

APOBEC-3G DeaminaseBiocatalysisCell ProliferationCells, CulturedCell SurvivalCytidine DeaminaseDNADNA RepairHumansKineticsPeptidesAPOBEC-3G DeaminaseAPOBEC3G protein, humanCytidine DeaminaseDNAPeptidesAPOBEC3GDNA bindingDNA repairlymphoma cellspeptides

Identifiers

PMID26460502
PMCPMC4712096
OpenAlexW2119255047

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.