ArticleScientific reports2017
Blood-testis barrier integrity depends on Pin1 expression in Sertoli cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Inflammation-Driven Remodeling of the Blood-Testis Barrier: Roles of Junctional Complexes, Actin Dynamics, and Kinase Signaling.Biomedicines · 2026Review
- A Comparison of White and Yellow Seminal Plasma Phosphoproteomes Obtained from Turkey (International journal of molecular sciences · 2024Article
- Common Variation in the PIN1 Locus Increases the Genetic Risk to Suffer from Sertoli Cell-Only Syndrome.Journal of personalized medicine · 2022Article
- Bibliometric and visual analysis of blood-testis barrier research.Frontiers in pharmacology · 2022Article
- Article
- Integrating miRNA and mRNA Profiling to Assess the Potential miRNA-mRNA Modules Linked With Testicular Immune Homeostasis in Sheep.Frontiers in veterinary science · 2021Article
- UXT in Sertoli cells is required for blood-testis barrier integrity†.Biology of reproduction · 2020Article
- "Frontiers in endocrinology · 2020Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The conformation and function of a subset of serine and threonine-phosphorylated proteins are regulated by the prolyl isomerase Pin1 through isomerization of phosphorylated Ser/Thr-Pro bonds. Pin1 is intensely expressed in Sertoli cells, but its function in this post mitotic cell remains unclear. Our aim was to investigate the role of Pin1 in the Sertoli cells. Lack of Pin1 caused disruption of the blood-testis barrier. We next investigated if the activin pathways in the Sertoli cells were affected by lack of Pin1 through immunostaining for Smad3 protein in testis tissue. Indeed, lack of Pin1 caused reduced Smad3 expression in the testis tissue, as well as a reduction in the level of N-Cadherin, a known target of Smad3. Pin1
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Registered trials
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