ArticleCell2010
Plzf regulates germline progenitor self-renewal by opposing mTORC1.
Article in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
150 citing papers in PubMed, 1 synthesis or guideline pooled it, 281 citations in OpenAlex.
- Metabolic transitions define spermatogonial stem cell maturation.Human reproduction (Oxford, England) · 2022Pooled it
- Review
- SMC1A is required for fate determinations of human spermatogonial stem cells and male fertility by interacting with YBX1 and stabilizing HMGA2 mRNA via an mCell death and differentiation · 2026Article
- Restoration of spermatogenesis is dependent on activation of a SPRY4-ERK checkpoint following germline stem cell damage†.Biology of reproduction · 2026Article
- A short PIWIL2 isoform PL2L60A induces functional and transcriptional changes indicative of a procancerous phenotype.Molecular biology reports · 2025Article
- Restoration of Spermatogenesis is Dependent on Activation of a SPRY4-ERK Checkpoint Following Germline Stem Cell Damage.bioRxiv : the preprint server for biology · 2025Article
- Effect of Extracellular Matrix Derived from Porcine Tissue on Stemness of Porcine Spermatogonial Stem Cells.International journal of molecular sciences · 2025Article
- Cnot3 is required for male germ cell development and spermatogonial stem cell maintenance.Development (Cambridge, England) · 2025Article
- ZBTB16/PLZF regulates juvenile spermatogonial stem cell development through an extensive transcription factor poising network.Nature structural & molecular biology · 2025Article
- Old versus new: upstream and downstream of promyelocytic leukemia zinc finger protein.Cancer gene therapy · 2025Review
- Utilization of the QuPath open-source software platform for analysis of mammalian spermatogenesis†.Biology of reproduction · 2025Article
- Altered Sertoli Cell Function Contributes to Spermatogenic Arrest in Dogs with Chronic Asymptomatic Orchitis.International journal of molecular sciences · 2025Article
- The Biology and Regulation of Spermatogonial Stem Cells in the Niche.Advances in experimental medicine and biology · 2025Review
- RGS14 binds to GNAI3 and regulates the proliferation and apoptosis of human spermatogonial stem cells by affecting PLPP2 expression and MAPK signaling.Frontiers in cell and developmental biology · 2025Article
- Article
- Genome-Wide Identification and Expression Analysis of theInternational journal of molecular sciences · 2024Article
- Autophagy accompanying the developmental process of male germline stem cells.Cell and tissue research · 2024Review
- PTN from Leydig cells activates SDC2 and modulates human spermatogonial stem cell proliferation and survival via GFRA1.Biological research · 2024Article
- EEF1B2 regulates the proliferation and apoptosis of human spermatogonial stem cell lines through TAF4B.Heliyon · 2024Article
- The Current and Future of Biomarkers of Immune Related Adverse Events.Rheumatic diseases clinics of North America · 2024Review
90 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Hyperactivity of mTORC1, a key mediator of cell growth, leads to stem cell depletion, although the underlying mechanisms are poorly defined. Using spermatogonial progenitor cells (SPCs) as a model system, we show that mTORC1 impairs stem cell maintenance by a negative feedback from mTORC1 to receptors required to transduce niche-derived signals. We find that SPCs lacking Plzf, a transcription factor essential for SPC maintenance, have enhanced mTORC1 activity. Aberrant mTORC1 activation in Plzf(-/-) SPCs inhibits their response to GDNF, a growth factor critical for SPC self-renewal, via negative feedback at the level of the GDNF receptor. Plzf opposes mTORC1 activity by inducing expression of the mTORC1 inhibitor Redd1. Thus, we identify the mTORC1-Plzf functional interaction as a critical rheostat for maintenance of the spermatogonial pool and propose a model whereby negative feedback from mTORC1 to the GDNF receptor balances SPC growth with self-renewal.
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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.