ArticleMolecular therapy : the journal of the American Society of Gene Therapy2014
Induction of androgen formation in the male by a TAT-VDAC1 fusion peptide blocking 14-3-3ɛ protein adaptor and mitochondrial VDAC1 interactions.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 44 citations in OpenAlex.
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- Age-related testosterone decline: mechanisms and intervention strategies.Reproductive biology and endocrinology : RB&E · 2024Review
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- VDAC1-Based Peptides as Potential Modulators of VDAC1 Interactions with Its Partners and as a Therapeutic for Cancer, NASH, and Diabetes.Biomolecules · 2024Review
- Mitochondrial control of microglial phagocytosis by the translocator protein and hexokinase 2 in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Oral administration of VDAC1-derived small molecule peptides increases circulating testosterone levels in male rats.Frontiers in endocrinology · 2022Article
- Differential mitochondrial protein interaction profile between human translocator protein and its A147T polymorphism variant.PloS one · 2022Article
- TSPO protein binding partners in bacteria, animals, and plants.Journal of bioenergetics and biomembranes · 2021Review
- Advances in stem cell research for the treatment of primary hypogonadism.Nature reviews. Urology · 2021Review
- Article
- High Throughput scRNA-Seq Provides Insights Into Leydig Cell Senescence Induced by Experimental Autoimmune Orchitis: A Prominent Role of Interstitial Fibrosis and Complement Activation.Frontiers in immunology · 2021Article
- Effects of pharmacologically induced Leydig cell testosterone production on intratesticular testosterone and spermatogenesis†.Biology of reproduction · 2020Article
- Identification of Sec23ip, Part of 14-3-3γ Protein Network, as a Regulator of Acute Steroidogenesis in MA-10 Leydig Cells.Endocrinology · 2020Article
- Article
- Assessing the role of residue E73 and lipid headgroup charge in VDAC1 voltage gating.Biochimica et biophysica acta. Bioenergetics · 2019Article
- A novel cell-penetrating peptide protects against neuron apoptosis after cerebral ischemia by inhibiting the nuclear translocation of annexin A1.Cell death and differentiation · 2019Article
- Leydig cells: formation, function, and regulation.Biology of reproduction · 2018Review
- Translocator protein (18 kDa): an update on its function in steroidogenesis.Journal of neuroendocrinology · 2018Review
- Adrenal Mitochondria and Steroidogenesis: From Individual Proteins to Functional Protein Assemblies.Frontiers in endocrinology · 2016Review
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5 authors at 2 institutions in 1 country.
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Abstract
Low testosterone (T), a major cause of male hypogonadism and infertility, is linked to mood changes, fatigue, osteoporosis, reduced bone-mass index, and aging. The treatment of choice, T replacement therapy, has been linked with increased risk for prostate cancer and luteinizing hormone (LH) suppression, and shown to lead to infertility, cardiovascular diseases, and obesity. Alternate methods to induce T with lower side effects are desirable. In search of the mechanisms regulating T synthesis in the testes, we identified the 14-3-3ɛ protein adaptor as a negative regulator of steroidogenesis. Steroidogenesis begins in mitochondria. 14-3-3ɛ interacts with the outer mitochondrial membrane voltage-dependent anion channel (VDAC1) protein, forming a scaffold that limits the availability of cholesterol for steroidogenesis. We report the development of a tool able to induce endogenous T formation. Peptides able to penetrate testes conjugated to 14-3-3ɛ site of interaction with VDAC1 blocked 14-3-3ɛ-VDAC1 interactions while at the same time increased VDAC1-translocator protein (18 kDa) interactions that induced steroid formation in rat testes, leading to increased serum T levels. These peptides rescued intratesticular and serum T formation in adult male rats treated with gonadotropin-releasing hormone antagonist, which dampened LH and T production.
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