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

Maintaining HNF6 expression prevents AdHNF3beta-mediated decrease in hepatic levels of Glut-2 and glycogen.

Yongjun Tan1, Guy Adami, Robert H Costa

  • 1Department of Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, IL 60607-7170, USA.

Hepatology (Baltimore, Md.)
|March 27, 2002
PubMed
Summary

Hepatocyte nuclear factor 3 (HNF-3) and HNF-6 transcription factors regulate liver gene expression. Maintaining HNF-6 during HNF-3beta infection restores glycogen and Glut-2 levels, showing HNF-6 directly activates the Glut-2 gene.

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

M1-NP1 interfering-peptide inhibits cancer cell proliferation and migration by targeting the transcription factor FOXM1.

Journal of pharmaceutical analysis·2026
Same author

Raw defines a TIR-fold cADPR hydrolase cooperating with dSarm in development and axon degeneration.

Cell communication and signaling : CCS·2026
Same author

Inactivation of a purine biosynthesis repressor promotes ribosome synthesis to overcome antibiotic stress.

mBio·2026
Same author

Vitamin B12 attenuates post-ischemic brain fibrotic remodeling and suppresses MAPK1 signaling in male rats.

Brain research bulletin·2026
Same author

Reversible DNA condensation drives natural transformation.

Nature communications·2026
Same author

The association between vitamin B12 and lipid metabolism in patients with ischemic stroke: A cross-sectional study.

Journal of clinical lipidology·2026

Area of Science:

  • Molecular Biology
  • Hepatology
  • Gene Regulation

Background:

  • Hepatocyte nuclear factor 3 (HNF-3) proteins, part of the Forkhead Box (Fox) family, are crucial for regulating genes involved in liver cell proliferation, differentiation, and metabolic balance.
  • Previous studies showed that increasing HNF-3beta in mouse liver reduced glycogen, glucose transporter 2 (Glut-2), and several transcription factors, including HNF-6.
  • The interplay between HNF-3 and HNF-6 in regulating hepatic gene expression, particularly concerning glycogen and Glut-2, remained unclear.

Purpose of the Study:

  • To investigate whether co-expression of HNF-6 can prevent the reduction of hepatic glycogen and Glut-2 levels observed during HNF-3beta overexpression.
  • To elucidate the role of HNF-6 in the transcriptional regulation of the Glut-2 gene in the liver.
  • To determine if HNF-6 directly binds to and activates the Glut-2 promoter.

Related Experiment Videos

Main Methods:

  • Adenovirus-mediated gene delivery was used to manipulate HNF-3beta and HNF-6 expression in mouse liver.
  • Hepatic levels of glycogen, Glut-2, and various transcription factors were quantified post-infection.
  • DNA binding assays and cotransfection experiments in HepG2 cells were performed to assess promoter binding and transcriptional activity.

Main Results:

  • Co-infection with AdHNF3beta and AdHNF6 increased hepatic glycogen, Glut-2, HNF-3gamma, HNF-1alpha, and HNF-4alpha levels.
  • HNF-6 infection alone significantly increased hepatic Glut-2 levels, indicating its role in stimulating Glut-2 transcription.
  • HNF-6, but not HNF-3 proteins, bound to the Glut-2 promoter (-185 to -144 bp) and activated its transcription in HepG2 cells.

Conclusions:

  • Maintaining HNF-6 expression during HNF-3beta overexpression prevents the decrease in hepatic glycogen and Glut-2.
  • The hepatic Glut-2 promoter is a direct transcriptional target of HNF-6.
  • HNF-6 plays a significant role in regulating glucose metabolism through direct activation of Glut-2 expression.