Related Experiment Video

Updated: Aug 11, 2025

Rescue of Recombinant Newcastle Disease Virus from cDNA
10:55

Rescue of Recombinant Newcastle Disease Virus from cDNA

Published on: October 11, 2013

19.4K

Chicken-derived MERTK protein inhibits Newcastle disease virus replication by increasing STAT1 phosphorylation in

Lei Tan1, Meizhen Huang2, Xusheng Qiu2

  • 1Department of Avian Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai 200241, China; Shanghai Key Laboratory of Veterinary Biotechnology, Shanghai, People's Republic of China.

Virus Research
|February 8, 2023
PubMed

Insights

Chicken Mertk protein enhances the type I interferon response against Newcastle disease virus (NDV). Casitas B-lineage proto-oncogene (CBL) negatively regulates Mertk, impacting STAT1 phosphorylation and antiviral activity.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Receptor tyrosine kinases TYRO3, AXL, and MERTK (TAM) are key regulators of innate immunity.
  • Newcastle disease virus (NDV) causes significant economic losses in the poultry industry worldwide.
  • Understanding the innate immune response to NDV is crucial for developing effective control strategies.

Purpose of the Study:

  • To investigate the role of chicken MERTK (chMertk) in regulating the type I interferon (IFN) signaling pathway.
  • To determine the antiviral effect of chMertk against NDV in vitro.
  • To elucidate the regulatory mechanism of chMertk by other cellular factors.

Main Methods:

  • Overexpression of exogenous chMertk in chicken cells.
  • Mutation assay to identify key tyrosine residues in chMertk.
  • Analysis of STAT1 phosphorylation and IFN-stimulated gene expression (IFITM3).
  • Measurement of NDV titer.
  • Investigation of chMertk regulation by chicken E3 ubiquitin ligase CBL and the effect of the proteasome inhibitor MG132.

Main Results:

  • Overexpression of chMertk upregulated STAT1 phosphorylation and IFITM3 expression, significantly reducing NDV titer.
  • Specific tyrosine residues (Y739, Y743, Y744) in chMertk were found to promote STAT1 phosphorylation and inhibit NDV replication.
  • Chicken CBL negatively regulated chMertk expression, attenuating STAT1 phosphorylation.
  • chMertk function was restored by MG132, indicating CBL-mediated ubiquitination and degradation of chMertk.

Conclusions:

  • chMertk plays a significant role in the innate immune response against NDV infection.
  • CBL negatively regulates chMertk expression via ubiquitination and degradation, contributing to cellular homeostasis.
  • These findings offer new insights into chMertk's function in innate immunity and its anti-NDV activity.
Keywords:
Casitas B-lineage proto-oncogene (CBL)MERTKNewcastle disease virus (NDV)Receptor tyrosine kinaseSignal transducer and activator of transcription 1 (STAT1)

More Related Videos

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.5K
Production of High-Titer Recombinant Newcastle Disease Virus from Allantoic Fluid07:24

Production of High-Titer Recombinant Newcastle Disease Virus from Allantoic Fluid

Published on: May 25, 2022

3.7K

Related Concept Videos

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...
9.1K