Evidence map›Paper›PMID 18802965›Full record

ArticleGenesis (New York, N.Y. : 2000)2008

Generation of a conditional null allele for Cftr in mice.

Craig A Hodges, Calvin U Cotton, Mark R Palmert, Mitchell L Drumm

Open access · greenAbstract read
In one paragraph

Article in Genesis (New York, N.Y. : 2000), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A W1282X cystic fibrosis mouse allows the study of pharmacological and gene-editing therapeutics to restore CFTR function.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Lower Expression ofCancers · 2023
    Article
  12. Article
  13. CFTR regulates brown adipocyte thermogenesis via the cAMP/PKA signaling pathway.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Enhancing Cystic Fibrosis Immune Regulation.Frontiers in pharmacology · 2021
    Article
  19. Article
  20. Impaired Renal HCOJournal of the American Society of Nephrology : JASN · 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

4 authors at 3 institutions in 2 countries.

Craig A HodgesDepartment of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
Calvin U Cotton
Mark R Palmert
Mitchell L Drumm
Case Western Reserve University · USSickKids Foundation · CAUniversity School · US

Funding

Translational Research in Cystic FibrosisP30DK027651 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI DRUMM, MITCHELL L · 1986 to 2014
$15.6M
Genetic Factors that Regulate the Onset of PubertyR01HD048960 · NICHD · HOSPITAL FOR SICK CHLDRN (TORONTO) · PI PALMERT, MARK R · 2005 to 2009
$1.9M
NICHD NIH HHS R01 HD048960NIDDK NIH HHS P30 DK027651
6 · The paper itself

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) gene encodes a cAMP-regulated chloride channel that is important in controlling the exchange of fluid and electrolytes across epithelial cells. Mutation of CFTR can lead to cystic fibrosis (CF), the most common lethal genetic disease in Caucasians. CF is a systemic illness with multiple organ systems affected including pulmonary, gastrointestinal, pancreatic, immune, endocrine, and reproductive systems. To understand the role of CFTR in the various tissues in which it is expressed, we generated a murine conditional null allele of Cftr (Cftr(fl10)) in which loxP sites were inserted around exon 10 of the Cftr gene. The Cftr(fl10) allele was validated by generating constitutive Cftr null (Cftr(Delta10)) mice using the protamine-cre system. The Cftr(Delta10/Delta10) mice displayed almost identical phenotypes to previously published CF mouse models, including poor growth, decreased survival, intestinal obstruction, and loss of Cftr function as assessed by electrophysiology measurements on gut and nasal epithelium. Mice containing the conditional null Cftr allele will be useful in future studies to understand the role of Cftr in specific tissues and developmental time points and lead to a better understanding of CF disease.

Indexed as

AllelesAnimalsCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDisease Models, AnimalElectrophysiological PhenomenaFemaleIntegrasesMaleMiceMice, Inbred C57BLMice, Inbred CFTRMice, KnockoutMice, TransgenicCre recombinaseCystic Fibrosis Transmembrane Conductance RegulatorIntegrases

Identifiers

PMID18802965
PMCPMC2711445
OpenAlexW1991262003

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.