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 Concept Videos

You might also read

Related Articles

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

Sort by
Same author

CRISPR activation of endogenous <i>PKD1</i> increases polycystin-1 levels and suppresses cellular features of ADPKD.

bioRxiv : the preprint server for biology·2026
Same author

Glucocorticoid receptor and RUNX transcription factors cooperatively drive CD8 T cell dysfunction in human cancer.

Cell reports·2026
Same author

Cortisol-resistant CAR-NK cells overcome steroid-induced immunosuppression in lung cancer.

Signal transduction and targeted therapy·2026
Same author

Polycystin-1 C-Terminus Regulates Protein Synthesis-Related Pathways in Cardiomyocytes.

bioRxiv : the preprint server for biology·2026
Same author

The Enamel Matrix Protein Amelogenin is Essential for Enamel Mineral Transport and Deposition.

Stem cells and development·2026
Same author

Enzymatic Remodelling of Tumour Microenvironment Enhances Anti-CEACAM5 CAR T-Cell Efficacy Against Colorectal Cancer.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Related Experiment Video

Updated: May 1, 2026

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
04:49

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome

Published on: July 5, 2024

1.9K

Case study: polycystic livers in a transgenic mouse line.

Jamie Lovaglio1, James E Artwohl2, Christopher J Ward3

  • 1Biologic Resources Laboratory, University of Illinois at Chicago, Chicago, Illinois, USA.

Comparative Medicine
|March 29, 2014
PubMed
Summary
This summary is machine-generated.

Polycystic liver disease in K14 transgenic mice caused infertility and testicular degeneration. This study details the pathology and reproductive failure in these mice.

More Related Videos

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
10:56

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes

Published on: September 15, 2018

7.5K
Author Spotlight: Evaluating Therapeutic Strategies to Enhance Liver Regeneration
05:25

Author Spotlight: Evaluating Therapeutic Strategies to Enhance Liver Regeneration

Published on: May 24, 2024

3.4K

Related Experiment Videos

Last Updated: May 1, 2026

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
04:49

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome

Published on: July 5, 2024

1.9K
A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
10:56

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes

Published on: September 15, 2018

7.5K
Author Spotlight: Evaluating Therapeutic Strategies to Enhance Liver Regeneration
05:25

Author Spotlight: Evaluating Therapeutic Strategies to Enhance Liver Regeneration

Published on: May 24, 2024

3.4K

Area of Science:

  • Hepatology
  • Reproductive Biology
  • Genetics

Background:

  • Mice transgenic for keratin 14 (K14)-driven LacZ expression were studied.
  • The study aimed to investigate a phenotype observed in these mice.

Observation:

  • Affected mice exhibited distended abdomens and enlarged livers with numerous cysts.
  • Histopathology confirmed hepatic cysts lined by biliary epithelium and mild chronic inflammation, with no parasites.
  • Five additional affected mice were identified among related individuals.

Findings:

  • Mice with polycystic livers failed to reproduce, with affected males showing testicular degeneration and immotile sperm.
  • Control K14 male mice without polycystic livers bred successfully and had normal sperm motility.
  • Genetic analysis did not link the phenotype to the transgene or its insertion site.

Implications:

  • The K14-driven LacZ transgene may be associated with polycystic liver disease and subsequent reproductive failure.
  • This mouse model offers a platform for studying the mechanisms of polycystic liver disease and its impact on reproduction.
  • Further research is needed to elucidate the genetic and molecular basis of this phenotype.