Evidence map›Paper›PMID 32015826›Full record

ReviewCell & bioscience2020

ATM, ATR and DNA-PKcs kinases-the lessons from the mouse models: inhibition ≠ deletion.

Demis Menolfi, Shan Zha

Open access · goldAbstract readReview
In one paragraph

Review in Cell & bioscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 1 pooled it
10.8field-weighted citation impact, top 1% 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

138 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.

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78 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.

Demis Menolfi1Institute for Cancer Genetics, College of Physicians & Surgeons, Columbia University, New York, NY 10032 USA.
Shan Zha1Institute for Cancer Genetics, College of Physicians & Surgeons, Columbia University, New York, NY 10032 USA.ORCID 0000-0002-6568-1818
Cancer Genetics (United States) · US

Funding

The role of ATM in the suppression of lymphoid malignancyR01CA158073 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Shan Zha · 2011 to 2026
$5.7M
DNA-PKCS Phosphorylation in DNA Repair and Chromosomal TranslocationsR01CA184187 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ZHA, SHAN · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA158073NCI NIH HHS R01 CA184187
6 · The paper itself

Abstract

DNA damage, especially DNA double strand breaks (DSBs) and replication stress, activates a complex post-translational network termed DNA damage response (DDR). Our review focuses on three PI3-kinase related protein kinases-ATM, ATR and DNA-PKcs, which situate at the apex of the mammalian DDR. They are recruited to and activated at the DNA damage sites by their respective sensor protein complexes-MRE11/RAD50/NBS1 for ATM, RPA/ATRIP for ATR and KU70-KU80/86 (XRCC6/XRCC5) for DNA-PKcs. Upon activation, ATM, ATR and DNA-PKcs phosphorylate a large number of partially overlapping substrates to promote efficient and accurate DNA repair and to coordinate DNA repair with other DNA metabolic events (

Indexed as

ATMATRDNA damage responseDNA-PKcsDouble-strand breaks (DSBs)Kinase inhibitionLymphocyte developmentSingle-strand DNA (ssDNA)

Identifiers

PMID32015826
PMCPMC6990542
OpenAlexW3007027724

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.