Regulation of CCL2 Gene Expression by LITAF and STAT6B
Author Information
Author(s): Tang Xiaoren, Yang Yu, Amar Salomon
Primary Institution: Center for Anti-inflammatory Therapeutics, School of Dental Medicine, Boston University, Boston, Massachusetts, United States of America
Hypothesis
The study investigates the role of the mLITAF/mSTAT6B complex in regulating CCL2 gene expression in response to LPS stimulation.
Conclusion
The mLITAF/mSTAT6B complex is crucial for the nuclear translocation that leads to the production of CCL2 and TNF-α in response to LPS.
Supporting Evidence
- The mLITAF/mSTAT6B complex is essential for the nuclear translocation required for CCL2 production.
- Knockdown of mSTAT6B significantly reduced CCL2 production in macrophages.
- LPS stimulation induced mLITAF and mSTAT6B expression in a MyD88-dependent manner.
- CCL2 promoter activity was significantly increased by the overexpression of both mLITAF and mSTAT6B.
- mSTAT6B does not directly bind to the CCL2 promoter but enhances mLITAF's regulatory effect.
Takeaway
This study shows that two proteins, mLITAF and mSTAT6B, work together to help the body produce important signals when it gets hurt.
Methodology
The study used murine models, including wild-type and genetically modified mice, to analyze the interactions between mLITAF and mSTAT6B and their effects on CCL2 expression.
Potential Biases
Potential bias in the interpretation of results due to reliance on specific genetic models.
Limitations
The study primarily focuses on murine models, which may not fully represent human responses.
Participant Demographics
C57BL-6 mice, including wild-type and various genetically modified strains.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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