Related Experiment Video
Updated: Jul 17, 2025

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
Published on: January 12, 2020
FAM76B regulates NF-κB-mediated inflammatory pathway by influencing the translocation of hnRNPA2B1
Dongyang Wang1,2, Xiaojing Zheng1, Lihong Chai1
1Laboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Xi'an, China.
Abstract:
FAM76B has been reported to be a nuclear speckle-localized protein with unknown function. In this study, FAM76B was first demonstrated to inhibit the NF-κB-mediated inflammatory pathway by affecting the translocation of hnRNPA2B1 in vitro. We further showed that FAM76B suppressed inflammation in vivo using a traumatic brain injury (TBI) mouse model. Lastly, FAM76B was shown to interact with hnRNPA2B1 in human tissues taken from patients with acute, organizing, and chronic TBI, and with different neurodegenerative diseases. The results suggested that FAM76B mediated neuroinflammation via influencing the translocation of hnRNPA2B1 in vivo during TBI repair and neurodegenerative diseases. In summary, we for the first time demonstrated the role of FAM76B in regulating inflammation and further showed that FAM76B could regulate the NF-κB-mediated inflammatory pathway by affecting hnRNPA2B1 translocation, which provides new information for studying the mechanism of inflammation regulation.
Insights
FAM76B protein inhibits inflammation by regulating hnRNPA2B1 translocation in traumatic brain injury and neurodegenerative diseases. This study reveals FAM76B
Area of Science:
- Molecular Biology
- Neuroscience
- Immunology
Background:
- FAM76B is a nuclear speckle protein with an undefined role.
- Inflammation is a key factor in traumatic brain injury (TBI) and neurodegenerative diseases.
Purpose of the Study:
- To elucidate the function of FAM76B in inflammatory pathways.
- To investigate FAM76B's role in TBI and neurodegenerative disease models.
Main Methods:
- In vitro assays to assess NF-κB pathway inhibition.
- In vivo studies using a mouse model of traumatic brain injury.
- Analysis of human tissue samples from TBI and neurodegenerative disease patients.
Main Results:
- FAM76B inhibits the NF-κB inflammatory pathway by affecting hnRNPA2B1 translocation.
- FAM76B suppresses inflammation in a mouse model of TBI.
- FAM76B interacts with hnRNPA2B1 in human tissues relevant to TBI and neurodegeneration.
Conclusions:
- FAM76B plays a crucial role in regulating neuroinflammation.
- FAM76B influences hnRNPA2B1 translocation, impacting inflammatory responses in TBI and neurodegenerative conditions.
- This research provides novel insights into inflammation mechanisms.
Related Concept Videos
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
Co-activators and Co-repressors
Regulation of Nuclear Protein Sorting
Regulation of the Unfolded Protein Response
Transducer Mechanism: Nuclear Receptors
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
The Unfolded Protein Response

