ArticleIranian journal of biotechnology2023
The PBX1/miR-141-miR-200a/EGR2/SOCS3 Axis; Integrative Analysis of Interaction Networks to Discover the Possible Mechanism of MiR-141 and MiR-200a-Mediated Th17 Cell Differentiation.
Article in Iranian journal of biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Pbx1 as a regulator of T-cell fate in autoimmunity.Frontiers in immunology · 2026Review
- Dairy: Friend or Foe? Bovine Milk-Derived Extracellular Vesicles and Autoimmune Diseases.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
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Abstract
Background: Overexpression of miR-141 and miR-200a is known to be associated with the differentiation of T helper 17 (Th17) cells, which are key players in the pathophysiology of autoimmune disorders. However, the function and governing mechanism of these two microRNAs (miRNAs) in Th17 cell skewing are poorly defined. Objectives: The aim of the present study was to identify the common upstream transcription factors and downstream target genes of miR-141 and miR-200a to obtain a better insight into the possible dysregulated molecular regulatory networks driving miR-141/miR-200a-mediated Th17 cell development. Materials and Methods: A consensus-based prediction strategy was applied for Results: According to our miRNA-based and gene-based interaction network analyses, Conclusions: These results indicate that activation of the PBX1/miR-141-miR-200a/EGR2/SOCS3 axis may promote Th17 cell development and, therefore, trigger or exacerbate Th17-mediated autoimmunity.
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