Evidence map›Paper›PMID 26537451›Full record

ArticleNature communications2015

Recombinase-based conditional and reversible gene regulation via XTR alleles.

Camila Robles-Oteiza, Sarah Taylor, Travis Yates, Michelle Cicchini, Brian Lauderback, Christopher R Cashman, Aurora A Burds, Monte M Winslow, Tyler Jacks, David M Feldser

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  13. Cre/eLife · 2022
    Article
  14. Article
  15. Review
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  17. Article
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  19. Review
  20. Cell-Type-Specific Gene Inactivation andThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    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

10 authors at 4 institutions in 1 country.

Camila Robles-OteizaDepartment of Cancer Biology, Abramson Family Cancer Research Institute and Perelman School of Medicine at the University of Pennsylvania, 421 Curie Boulevard, 751 Biomedical Research Building II/III, Philadelphia, Pennsylvania 19004, USA.
Sarah TaylorKoch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, Cambridge, Massachusetts 02144, USA.
Travis YatesDepartment of Cancer Biology, Abramson Family Cancer Research Institute and Perelman School of Medicine at the University of Pennsylvania, 421 Curie Boulevard, 751 Biomedical Research Building II/III, Philadelphia, Pennsylvania 19004, USA.
Michelle CicchiniDepartment of Cancer Biology, Abramson Family Cancer Research Institute and Perelman School of Medicine at the University of Pennsylvania, 421 Curie Boulevard, 751 Biomedical Research Building II/III, Philadelphia, Pennsylvania 19004, USA.
Brian LauderbackDepartment of Cancer Biology, Abramson Family Cancer Research Institute and Perelman School of Medicine at the University of Pennsylvania, 421 Curie Boulevard, 751 Biomedical Research Building II/III, Philadelphia, Pennsylvania 19004, USA.
Christopher R CashmanKoch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, Cambridge, Massachusetts 02144, USA.
Aurora A BurdsKoch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, Cambridge, Massachusetts 02144, USA.
Monte M WinslowDepartment of Genetics, Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
Tyler JacksKoch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, Cambridge, Massachusetts 02144, USA.
David M FeldserDepartment of Cancer Biology, Abramson Family Cancer Research Institute and Perelman School of Medicine at the University of Pennsylvania, 421 Curie Boulevard, 751 Biomedical Research Building II/III, Philadelphia, Pennsylvania 19004, USA.
Massachusetts Institute of Technology · USUniversity of Pennsylvania · USCancer Research Institute · USStanford University · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Jacqueline A. Lees · 1985 to 2026
$93.9M
TRAINING PROGRAM IN CELL AND MOLECULAR BIOLOGYT32GM007229 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BARTOLOMEI, MARISA S. · 1985 to 2023
$14.0M
p53-Mediated Tumor Immune SurveillanceR01CA193602 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FELDSER, DAVID · 2015 to 2019
$2.0M
Molecular Dissection of Lung Cancer Progression and MetastasisR01CA175336 · NCI · STANFORD UNIVERSITY · PI WINSLOW, MONTE MEIER · 2013 to 2017
$1.7M
Establishing therapeutic efficacy and uncovering mechanisms of tumor suppressionR00CA158581 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FELDSER, DAVID · 2013 to 2015
$707k
Establishing therapeutic efficacy and uncovering mechanisms of tumor suppressionK99CA158581 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FELDSER, DAVID · 2011 to 2012
$233k
Howard Hughes Medical InstituteNCI NIH HHS K99 CA158581NCI NIH HHS P30 CA014051NCI NIH HHS P30 CA016520NCI NIH HHS P30-CA016520NCI NIH HHS P30-CA14051NCI NIH HHS R00 CA158581NCI NIH HHS R00-CA158581NCI NIH HHS R01 CA175336NCI NIH HHS R01-CA175336NCI NIH HHS R01 CA193602NIGMS NIH HHS T32 GM007229NIGMS NIH HHS T32-GM07229
6 · The paper itself

Abstract

Synthetic biological tools that enable precise regulation of gene function within in vivo systems have enormous potential to discern gene function in diverse physiological settings. Here we report the development and characterization of a synthetic gene switch that, when targeted in the mouse germline, enables conditional inactivation, reports gene expression and allows inducible restoration of the targeted gene. Gene inactivation and reporter expression is achieved through Cre-mediated stable inversion of an integrated gene-trap reporter, whereas inducible gene restoration is afforded by Flp-dependent deletion of the inverted gene trap. We validate our approach by targeting the p53 and Rb genes and establishing cell line and in vivo cancer model systems, to study the impact of p53 or Rb inactivation and restoration. We term this allele system XTR, to denote each of the allelic states and the associated expression patterns of the targeted gene: eXpressed (XTR), Trapped (TR) and Restored (R).

Indexed as

Gene Expression Regulation, NeoplasticGene SilencingGenes, p53Genes, RetinoblastomaAllelesAnimalsCell Line, TumorDisease Models, AnimalElectroporationEmbryo, MammalianEpithelial CellsFibroblastsGenes, ReporterGenes, SyntheticGerm-Line MutationIntegrasesCre recombinaseIntegrases

Identifiers

PMID26537451
PMCPMC4635517
OpenAlexW2256348624

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.