Evidence map›Paper›PMID 32797168›Full record

ArticleNucleic acids research2020

A multiplexed bioluminescent reporter for sensitive and non-invasive tracking of DNA double strand break repair dynamics in vitro and in vivo.

Jasper Che-Yung Chien, Elie Tabet, Kelsey Pinkham, Cintia Carla da Hora, Jason Cheng-Yu Chang, Steven Lin, Christian E Badr, Charles Pin-Kuang Lai

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-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

14 citing papers in PubMed, 20 citations in OpenAlex.

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  6. CRM1 regulates androgen receptor stability and impacts DNA repair pathways in prostate cancer, independent of the androgen receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

8 authors at 5 institutions in 2 countries.

Jasper Che-Yung ChienInstitute of Atomic and Molecular Sciences, Academia Sinica, Taipei 10617, Taiwan.
Elie TabetDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA.
Kelsey PinkhamDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA.
Cintia Carla da HoraDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA.
Jason Cheng-Yu ChangInstitute of Biochemical Sciences, National Taiwan University, Taipei 10617, Taiwan.
Steven LinInstitute of Biochemical Sciences, National Taiwan University, Taipei 10617, Taiwan.
Christian E BadrDepartment of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA.
Charles Pin-Kuang LaiInstitute of Atomic and Molecular Sciences, Academia Sinica, Taipei 10617, Taiwan.
National Taiwan University · TWHarvard University · USInstitute of Atomic and Molecular Sciences, Academia Sinica · TWMassachusetts General Hospital · USUniversity of South Dakota · US

Funding

Identifying vulnerabilities and therapeutic targets in Glioma Stem CellsK22CA197053 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI BADR, CHRISTIAN ELIAS · 2015 to 2017
$603k
NCI NIH HHS K22 CA197053
6 · The paper itself

Abstract

Tracking DNA double strand break (DSB) repair is paramount for the understanding and therapeutic development of various diseases including cancers. Herein, we describe a multiplexed bioluminescent repair reporter (BLRR) for non-invasive monitoring of DSB repair pathways in living cells and animals. The BLRR approach employs secreted Gaussia and Vargula luciferases to simultaneously detect homology-directed repair (HDR) and non-homologous end joining (NHEJ), respectively. BLRR data are consistent with next-generation sequencing results for reporting HDR (R2 = 0.9722) and NHEJ (R2 = 0.919) events. Moreover, BLRR analysis allows longitudinal tracking of HDR and NHEJ activities in cells, and enables detection of DSB repairs in xenografted tumours in vivo. Using the BLRR system, we observed a significant difference in the efficiency of CRISPR/Cas9-mediated editing with guide RNAs only 1-10 bp apart. Moreover, BLRR analysis detected altered dynamics for DSB repair induced by small-molecule modulators. Finally, we discovered HDR-suppressing functions of anticancer cardiac glycosides in human glioblastomas and glioma cancer stem-like cells via inhibition of DNA repair protein RAD51 homolog 1 (RAD51). The BLRR method provides a highly sensitive platform to simultaneously and longitudinally track HDR and NHEJ dynamics that is sufficiently versatile for elucidating the physiology and therapeutic development of DSB repair.

Indexed as

Genes, ReporterRecombinational DNA RepairAnimalsCell Line, TumorCopepodaCRISPR-Cas SystemsDNA End-Joining RepairFemaleHEK293 CellsHigh-Throughput Nucleotide SequencingHumansLuciferasesMiceMice, NudeMultiplex Polymerase Chain ReactionOptical ImagingLuciferasesRAD51 protein, humanRad51 Recombinase

Identifiers

PMID32797168
PMCPMC7515717
OpenAlexW3049256974

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.