ArticleCell proliferation2022
Analysis of chromatin accessibility in p53 deficient spermatogonial stem cells for high frequency transformation into pluripotent state.
Article in Cell proliferation, 2022. 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, 34 citations in OpenAlex.
- SMAD3 and HIF-1α orchestrate metabolic transition to aerobic glycolysis as a critical prerequisite for spontaneous reprogramming of spermatogonial stem cells.Stem cell research & therapy · 2025Article
- From unipotency to pluripotency: deciphering protein networks and signaling pathways in the generation of embryonic stem-like cells from murine spermatogonial stem cells.BMC genomics · 2025Article
- Androgen blockage impairs proliferation and function of Sertoli cells via Wee1 and Lfng.Cell communication and signaling : CCS · 2024Article
- Expression profiling of stemness markers in testicular germline stem cells from neonatal and adult Swiss albino mice during their transdifferentiation in vitro.Stem cell research & therapy · 2024Article
- A rapid and stable spontaneous reprogramming system of Spermatogonial stem cells to Pluripotent State.Cell & bioscience · 2023Article
- BMI1 fine-tunes gene repression and activation to safeguard undifferentiated spermatogonia fate.Frontiers in cell and developmental biology · 2023Article
- Regulation of male germline transmission patterns by the Trp53-Cdkn1a pathway.Stem cell reports · 2022Article
- Analysis of chromatin accessibility in p53 deficient spermatogonial stem cells for high frequency transformation into pluripotent state.Cell proliferation · 2022Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
objectivesSpermatogonial stem cells (SSCs), the germline stem cells (GSCs) committed to spermatogenesis in niche, can transform into pluripotent state in long-term culture without introduction of exogenous factors, typically in p53 deficiency condition. As the guardian for genomic stability, p53 is associated with epigenetic alterations during SSCs transformation. However, the mechanism is still unknown, since complicated roles of p53 baffle our understanding of the regulating process. MATERIALS AND
methodsThe chromatin accessibility and differentially expressed genes (DEGs) were analysed in p53
resultsSeveral transcription factors (TFs), such as CTCF, SMAD3 and SOX2, were predicted as important factors mediating the transformation. Molecular evidence suggested that SMAD3 efficiently promoted pluripotency-associated gene expression both in fresh and long-term cultured SSCs. However, p53 knockout (KO) is insufficient to induce SMAD3 expression in SSCs.
conclusionsThese observations indicate that SMAD3 is a key factor for SSCs transformation, and an unknown event is required to activate SMAD3 as the prerequisite for SSCs reprogramming, which may occur in the long-term culture of SSCs. This study demonstrates the connection of p53 and pluripotency-associated factors, providing new insight for understanding the mechanisms of SSCs reprogramming and germline tumorigenesis.
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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 Socratic graph.