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Published on: January 27, 2021
Regulation of Paneth Cell Function by RNA-Binding Proteins and Noncoding RNAs
Hee K Chung1,2, Lan Xiao1,2, Krishna C Jaladanki1
1Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Paneth cells maintain gut homeostasis and stem cell niches. Dysregulation of RNA-binding proteins (RBPs) and noncoding RNAs (ncRNAs), like HuR and H19, impairs Paneth cell function, contributing to gut diseases.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Paneth cells are crucial for gut homeostasis, acting as a barrier against bacterial translocation and supporting intestinal stem cells.
- Recent research highlights Paneth cells' role in epithelium-microbiome interactions and gut inflammation pathogenesis.
- Paneth cell dysfunction is linked to various human gut mucosal diseases.
Purpose of the Study:
- To review the posttranscriptional regulation of Paneth cells by RNA-binding proteins (RBPs) and noncoding RNAs (ncRNAs).
- To focus on the roles of RBP HuR and long ncRNA H19 in Paneth cell function.
- To discuss how disrupted HuR and H19 expression contributes to Paneth cell dysfunction and gut pathologies.
Main Methods:
- Literature review focusing on posttranscriptional regulation mechanisms.
- Analysis of studies investigating RBPs and ncRNAs in Paneth cell biology.
- Examination of evidence linking HuR and H19 to Paneth cell function and disease.
Main Results:
- Posttranscriptional regulation by RBPs and ncRNAs significantly impacts Paneth cell function.
- RBP HuR and long ncRNA H19 are key players in modulating Paneth cell activity.
- Disrupted expression of HuR and H19 leads to Paneth cell defects and increased susceptibility to gut inflammation and infection.
Conclusions:
- RBPs and ncRNAs are critical regulators of Paneth cell function.
- HuR and H19 are implicated in maintaining gut health through Paneth cell regulation.
- Targeting HuR and H19 pathways may offer therapeutic strategies for gut mucosal diseases.
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