ArticleReproductive toxicology (Elmsford, N.Y.)2019
mTORC1/rpS6 and spermatogenic function in the testis-insights from the adjudin model.
Article in Reproductive toxicology (Elmsford, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- The relationship between sperm secretion and the Hippo signaling pathway in the rat seminiferous tubules.Scientific reports · 2025Article
- Testicular immunity.Molecular aspects of medicine · 2024Review
- RpL38 modulates germ cell differentiation by controlling Bam expression in Drosophila testis.Science China. Life sciences · 2024Article
- Exploring the pharmacological mechanism of Shengjing capsule on male infertility by a network pharmacology approach.BMC complementary medicine and therapies · 2022Article
- KIF15 supports spermatogenesis via its effects on Sertoli cell microtubule, actin, vimentin, and septin cytoskeletons.Endocrinology · 2021Article
- Microtubule-associated proteins (MAPs) in microtubule cytoskeletal dynamics and spermatogenesis.Histology and histopathology · 2021Review
- The Non-hormonal Male Contraceptive Adjudin Exerts its Effects via MAPs and Signaling Proteins mTORC1/rpS6 and FAK-Y407.Endocrinology · 2021Article
- Microtubule Cytoskeleton and Spermatogenesis-Lesson From Studies of Toxicant Models.Toxicological sciences : an official journal of the Society of Toxicology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
mTORC1/rpS6 signaling complex promoted Sertoli blood-testis barrier (BTB) remodeling by perturbing Sertoli cell-cell adhesion site known as the basal ectoplasmic specialization (ES). mTORC1/rpS6 complex also promoted disruption of spermatid adhesion at the Sertoli-spermatid interface called the apical ES. Herein, we performed analyses using the adjudin (a non-hormonal male contraceptive drug under development) model, wherein adjudin was known to perturb apical and basal ES function when used at high dose. Through direct administration of adjudin to the testis, adjudin at doses that failed to perturb BTB integrity per se, overexpression of an rpS6 phosphomimetic (i.e., constitutively active) mutant (i.e., p-rpS6-MT) that modified BTB function considerably potentiated adjudin efficacy. This led to disorderly spatial expression of proteins necessary to maintain the proper cytoskeletal organization of F-actin and microtubules (MTs) across the seminiferous epithelium, leading to germ cell exfoliation and aspermatogenesis. These findings yielded important insights regarding the role of mTORC1/rpS6 signaling complex in regulating BTB homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.