Related Experiment Video

Updated: Dec 13, 2025

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury
07:27

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury

Published on: October 21, 2017

12.2K

Mitochondrial protein UCP1 mediates liver injury induced by LPS through EKR signaling pathway

P Liu1, J Yang, Z-Y Chen

  • 1Department of Cadre Health Care, Qingdao Municipal Hospital, Qingdao, Shandong, China.

European Review for Medical and Pharmacological Sciences
|July 25, 2020
PubMed

Insights

This study on mitochondrial protein UCP1 and liver injury has been withdrawn due to suspected research misconduct. The publisher retracted the article as authors could not verify data originality.

Area of Science:

  • Biochemistry
  • Immunology
  • Pharmacology

Background:

  • Mitochondrial uncoupling protein 1 (UCP1) plays a role in cellular energy metabolism.
  • Liver injury can be triggered by lipopolysaccharide (LPS), a component of Gram-negative bacteria.
  • Extracellular signal-regulated kinases (ERK) signaling pathways are involved in cellular responses to stress and injury.

Purpose of the Study:

  • To investigate the role of mitochondrial UCP1 in LPS-induced liver injury.
  • To elucidate the involvement of the ERK signaling pathway in this process.

Main Methods:

  • The study likely involved in vitro or in vivo models to assess liver injury.
  • Techniques may have included Western blotting, gene expression analysis, or histological examination.
  • Specific inhibitors or activators of UCP1 and ERK pathways might have been used.

Main Results:

  • The original study suggested that UCP1 mediates LPS-induced liver injury.
  • It indicated that the ERK signaling pathway is involved in this mediation.
  • Specific findings regarding the interaction between UCP1, LPS, and ERK were presented.

Conclusions:

  • The original findings suggested UCP1 as a key mediator in LPS-induced liver injury via the ERK pathway.
  • The study aimed to provide a molecular understanding of liver damage in response to bacterial components.

More Related Videos

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

1.3K
Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice08:32

Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice

Published on: March 10, 2017

10.4K

Related Concept Videos

The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
6.0K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
2.8K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.0K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
9.6K
Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
4.8K