ArticleCell cycle (Georgetown, Tex.)2018
Interplay between p53 and Ink4c in spermatogenesis and fertility.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- The Impact of Different Equilibration Methods on the Cryopreservation Effectiveness of Boar Semen.Veterinary medicine and science · 2026Review
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- The role of p53 in male infertility.Frontiers in endocrinology · 2024Review
- Regulation of male germline transmission patterns by the Trp53-Cdkn1a pathway.Stem cell reports · 2022Article
- Comparison betweenInternational journal of fertility & sterility · 2022Article
- Testicular Localization and Potential Function of Vimentin Positive Cells during Spermatogonial Differentiation Stages.Animals : an open access journal from MDPI · 2022Article
- Wuzi Yanzong Pill-Based on Network Pharmacology andFrontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53, and the cyclin-dependent kinase inhibitor Ink4c, have been both implicated in spermatogenesis control. Both p53-/- and Ink4c-/- single knockout male mice are fertile, despite testicular hypertrophy, Leydig cell differentiation defect, and increased sperm count in Ink4c-/- males. To investigate their collaborative roles, we studied p53-/- Ink4c-/- dual knockout animals, and found that male p53-/- Ink4c-/- mice have profoundly reduced fertility. Dual knockout male mice show a marked decrease in sperm count, abnormal sperm morphology and motility, prolongation of spermatozoa proliferation and delay of meiosis entry, and accumulation of DNA damage. Genetic studies showed that the effects of p53 loss on fertility are independent of its downstream effector Cdkn1a. Absence of p53 also partially reverses the hyperplasia seen upon Ink4c loss, and normalizes the Leydig cell differentiation defect. These results implicate p53 in mitigating both the delayed entry into meiosis and the secondary apoptotic response that occur in the absence of Ink4c. We conclude that the cell cycle genes p53 and Ink4c collaborate in sperm cell development and differentiation, and may be important candidates to investigate in human male infertility conditions.
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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 OpenQuestion graph.