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

Mismatch Repair01:20

Mismatch Repair

4.8K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
4.8K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
MicroRNAs01:22

MicroRNAs

3.0K
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.0K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

4.7K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
4.7K
Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

10.6K
The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
Usually, Upf3 binds to an Exon Junction Complex (EJC) at mRNA splice sites. If a ribosome fully translates the mRNA,...
10.6K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.1K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.1K

You might also read

Related Articles

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

Sort by
Same author

Improved prognostic survival models for pediatric medulloblastoma using high dimensional gene expression data.

BMC medical genomics·2026
Same author

Calpain-4 Knockdown Modulates Cholesterol Metabolism and LXRα Nuclear Localization in Experimental Alcohol-Related Liver Disease.

Alcohol, clinical & experimental research·2026
Same author

Mean Arterial Pressure at Admission Predicts 28-day Mortality in Patients with Severe Alcohol-associated Hepatitis.

Clinical and translational gastroenterology·2026
Same author

α-Diversity analysis of hepatic transcriptome reveals distinct pathways in alcohol-associated hepatitis.

JCI insight·2026
Same author

Alpha diversity analysis of hepatic transcriptome reveals novel pathways in alcohol-related hepatitis.

bioRxiv : the preprint server for biology·2025
Same author

Calpain-4 Knockdown Modulates Cholesterol Metabolism and LXRα Nuclear Localization in Alcohol-Related Liver Disease.

bioRxiv : the preprint server for biology·2025
Same journal

Correction: Establishment of a Cre-rat resource for creating conditional and physiological relevant models of human diseases.

Transgenic research·2026
Same journal

Effects of CRISPR technology on agricultural sustainability: global applications and turkish perspective.

Transgenic research·2026
Same journal

Mammalian growth factors enhance regeneration in transgenic tomato lines.

Transgenic research·2026
Same journal

Transgenic expression of human signal regulatory protein alpha (SIRPα) in BALB/c Rag2<sup>null</sup>/Jak3<sup>null</sup> immunodeficient mice enhances human lymphoma xenografts by reducing phagocytosis.

Transgenic research·2026
Same journal

Evaluation of different mutagens in tuberose (Polianthes tuberosa) cut flower.

Transgenic research·2026
Same journal

Suppressor activity against cosuppression conferred by the petunia vein clearing virus genome.

Transgenic research·2026
See all related articles

Related Experiment Video

Updated: Jun 13, 2025

TGF-&#946;-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
07:05

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

5.1K

NORE1A loss promotes MASLD/MASH.

Howard Donninger1, Katherine Hobbing2, Gavin E Arteel3

  • 1Department of Medicine, University of Louisville, Louisville, KY, USA.

Transgenic Research
|September 9, 2024
PubMed
Summary
This summary is machine-generated.

Loss of NORE1A, a tumor suppressor, promotes fatty liver disease (MASLD/MASH) by upregulating SREBP1. NORE1A deficiency may drive human MASLD, and NORE1A knockout mice offer a new disease model.

Keywords:
MASHMASLDNORE1ARASSF5

More Related Videos

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.4K
Loss- and Gain-of-function Approach to Investigate Early Cell Fate Determinants in Preimplantation Mouse Embryos
08:43

Loss- and Gain-of-function Approach to Investigate Early Cell Fate Determinants in Preimplantation Mouse Embryos

Published on: June 6, 2016

8.8K

Related Experiment Videos

Last Updated: Jun 13, 2025

TGF-&#946;-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
07:05

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

5.1K
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.4K
Loss- and Gain-of-function Approach to Investigate Early Cell Fate Determinants in Preimplantation Mouse Embryos
08:43

Loss- and Gain-of-function Approach to Investigate Early Cell Fate Determinants in Preimplantation Mouse Embryos

Published on: June 6, 2016

8.8K

Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • NORE1A (RASSF5) functions as a tumor suppressor and is often downregulated in liver cancer.
  • It acts upstream in the HIPPO pathway, crucial for liver development and metabolism.
  • HIPPO pathway disruption is linked to the pathogenesis of metabolic-associated steatotic liver disease (MASLD) and metabolic-associated steatohepatitis (MASH).

Purpose of the Study:

  • To investigate the role of NORE1A in the development of liver disease, particularly MASLD/MASH.
  • To explore the potential of NORE1A knockout mice as a model for human MASLD/MASH.

Main Methods:

  • Phenotypic analysis of NORE1A knockout mice.
  • Assessment of NORE1A knockdown effects on sterol regulatory element-binding protein 1 (SREBP1) expression in liver cells.
  • Correlation analysis of NORE1A protein and TAZ expression in human MASLD samples.

Main Results:

  • NORE1A knockout mice did not develop liver tumors but showed a strong propensity for fatty liver, characteristic of MASLD/MASH.
  • NORE1A knockdown in liver cells led to increased SREBP1 expression, a key factor in MASLD development.
  • Human MASLD samples exhibited an inverse correlation between NORE1A protein and TAZ expression.

Conclusions:

  • Loss of NORE1A expression may contribute to the pathogenesis of MASLD/MASH in humans.
  • NORE1A knockout mice represent a potential new preclinical model for studying human MASLD/MASH.
  • Understanding NORE1A's role could reveal new therapeutic targets for fatty liver diseases.