Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Functional enhancement of CFTR expression by mitomycin C.

R Maitra1, C M Shaw, B A Stanton

  • 1Department of Pharmacology & Toxicology, Dartmouth Medical School, Hanover NH 03755-3835, USA.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|March 29, 2001
PubMed
Summary

Mitomycin C (MMC) increases cystic fibrosis transmembrane conductance regulator (CFTR) expression and function. This finding offers potential for new therapeutic strategies for cystic fibrosis by enhancing chloride secretion.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cutting Waste in Bronchoscopy: A Multicenter Observational Study in the German Health Care System.

Chest·2026
Same author

Understanding the mechanisms underlying cognitive control in psychosis.

Psychological medicine·2024
Same author

Placenta Prævia with Mal-presentation-Hysterotomy for Rigid Os Uteri.

Daniel's Texas medical journal·2023
Same author

Urethral Caruncle, Their Treatment.

Daniel's Texas medical journal·2023
Same author

Hepatosplenic Candidiasis, its Treatment and Effect on Remission Status in Patients with Acute Leukaemia-a Report of Five Cases.

Hematology (Amsterdam, Netherlands)·2016
Same author

A dissociation of structure and function in the auditory cortex of patients with schizophrenia.

Acta neuropsychiatrica·2016

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Pharmacology

Background:

  • Cystic fibrosis (CF) stems from mutations in the CFTR gene, most commonly DeltaF508.
  • The DeltaF508 mutation causes CFTR protein misfolding, ER retention, and degradation, hindering its function.

Purpose of the Study:

  • To identify compounds that enhance CFTR biogenesis and trafficking.
  • To explore novel therapeutic strategies for cystic fibrosis.

Main Methods:

  • Utilized T-84 and HT-29 cell lines to study CFTR expression and function.
  • Investigated the effect of mitomycin C (MMC) on CFTR mRNA and protein levels.
  • Assessed chloride secretion in response to MMC treatment.

Main Results:

Related Experiment Videos

  • Mitomycin C (MMC) significantly increased CFTR mRNA and protein expression at low, non-cytotoxic concentrations (0.1 microM).
  • MMC treatment led to enhanced chloride secretion in treated cell lines.
  • The observed effects suggest MMC can promote CFTR biogenesis and trafficking.

    • Conclusions:

    • Mitomycin C (MMC) demonstrates potential as a therapeutic agent for cystic fibrosis.
    • MMC may serve as a valuable tool for understanding CFTR regulation and biogenesis.
    • Further research into MMC's mechanism could lead to improved CFTR-targeted therapies.