Evidence map›Paper›PMID 22935533›Full record

ReviewCirculation research2012

Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.

Jennifer Davis, Marjorie Maillet, Joseph M Miano, Jeffery D Molkentin

Abstract readReview
In one paragraph

Review in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
–field-weighted citation impact
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

77 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. A perspective of lipid nanoparticles for RNA delivery.Exploration (Beijing, China) · 2024
    Article
  10. Article
  11. Article
  12. Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. A human FLII gene variant alters sarcomeric actin thin filament length and predisposes to cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Article

17 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

4 authors.

Jennifer DavisDepartment of Pediatrics, University of Cincinnati, Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, 240 Albert Sabin Way, S4.409, Cincinnati, OH 45229, USA.
Marjorie Maillet
Joseph M Miano
Jeffery D Molkentin

Funding

WNT/^-catenin Signaling and Cardiac Fibrosis P01HL069779 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI JAMES, JEANNE M · 2002 to 2017
$27.0M
PKCa Signaling Regulates Contractility and Heart FailureP50HL077101 · NHLBI · UNIVERSITY OF CINCINNATI · PI MOLKENTIN, JEFFERY D · 2005 to 2009
$19.1M
PKC alpha as a translational target in Heart FailureP01HL108806 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RABINOWITZ, JOSEPH E · 2012 to 2016
$11.3M
VENTRICULAR MYOSIN LIGHT CHAIN 2 FUNCTION IN NORMAL AND FAILING HEARTSP50HL052318 · NHLBI · UNIVERSITY OF CINCINNATI · PI DORN, GERALD W. · 1995 to 2004
$8.8M
Thrombospondin 4 regulates adaptive ER stress responseRenewal - Resubmission - 1R01HL105924 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Jeffery D Molkentin · 2011 to 2026
$7.3M
CARDIAC HYPERTROPHIC INTRACELLULAR SIGNALING PATHWAYSR01HL062927 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ROBBINS, JEFFREY · 1999 to 2013
$3.9M
Molecular Pathways Controlling Cardiac Gene ExpressionR37HL060562 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 2008 to 2017
$3.8M
Howard Hughes Medical InstituteNHLBI NIH HHS P01 HL069779NHLBI NIH HHS P01 HL108806NHLBI NIH HHS P50 HL052318NHLBI NIH HHS P50 HL077101NHLBI NIH HHS R01 HL062927NHLBI NIH HHS R01 HL105924NHLBI NIH HHS R37 HL060562
6 · The paper itself

Abstract

The advent of modern mouse genetics has benefited many fields of diseased-based research over the past 20 years, none perhaps more profoundly than cardiac biology. Indeed, the heart is now arguably one of the easiest tissues to genetically manipulate, given the availability of an ever-growing tool chest of molecular reagents/promoters and "facilitator" mouse lines. It is now possible to modify the expression of essentially any gene or partial gene product in the mouse heart at any time, either gain or loss of function. This review is designed as a handbook for the nonmouse geneticist and/or junior investigator to permit the successful manipulation of any gene or RNA product in the heart, while avoiding artifacts. In the present review, guidelines, pitfalls, and limitations are presented so that rigorous and appropriate examination of cardiac genotype-phenotype relationships can be performed. This review uses examples from the field to illustrate the vast spectrum of experimental and design details that must be considered when using genetically modified mouse models to study cardiac biology.

Indexed as

Disease Models, AnimalAnimalsBiomedical ResearchGuidelines as TopicHeartHumansMiceMice, KnockoutMice, TransgenicMyocardium

Identifiers

PMID22935533
PMCPMC3466061

What OpenQuestion holds

Textmetadata
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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.