ArticleConnective tissue research2021
A retrotransposon gag-like-3 gene RTL3 and SOX-9 co-regulate the expression of COL2A1 in chondrocytes.
Article in Connective tissue research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Engineered Chondrocalcin From Pichia pastoris: A Dual-Functional Biomaterial for Cartilage Regeneration and Rheumatoid Arthritis Modulation.Biotechnology and bioengineering · 2026Article
- Partial meniscus allograft transplantation preserving the recipient's anterior root: a comparative study in a rabbit model.European journal of medical research · 2025Article
- Intercellular Communication in the Nervous System Goes Viral.Trends in neurosciences · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTransposable elements are known to remodel gene structure and provide a known source of genetic variation. Retrotransposon gag-like-3 (RTL3) is a mammalian retrotransposon-derived transcript ( MATERIALS AND
methodsExpression of
resultsRTL3 is not ubiquitously expressed but showed strong expression in cartilage, chondrocytes and synoviocytes but not in muscle, brain, or other tissues analyzed. Loss-of-function and gain-of-function studies demonstrated a critical role of RTL3 in the regulation of SOX-9 and COL2A1 expression and matrix synthesis during chondrogenesis. Both RTL3 and SOX-9 displayed co-regulated expression in chondrocytes. Gene regulatory activity of RTL3 requires the c-terminal CCHC zinc-finger binding domain.
conclusionsOur results identify a novel regulatory mechanism of COL2A1 expression in chondrocytes that may help to further understand the skeletal development and the pathogenesis of diseases with altered COL2A1 expression.
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Registered trials
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