Related Experiment Video

Updated: May 12, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
09:03

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Published on: February 3, 2012

Ursodeoxycholic acid inhibits feline infectious peritonitis virus infection through activating JAK-STAT signaling

Yi Zhong1, Zhiwei Sun1, Ziyan Song1

  • 1College of Veterinary Medicine, Southwest University, Chongqing, China.

Microbiology Spectrum
|May 11, 2026
PubMed

Keywords:
JAK-STAT signaling pathwayfeline infectious peritonitis viruslentivirusstable cell lineursodeoxycholic acid

More Related Videos

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro14:18

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

Published on: October 13, 2023

Related Concept Videos

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Acute Pancreatitis I: Introduction01:25

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...