ArticleMolecular and cellular biology2001
Control of spermatogenesis in mice by the cyclin D-dependent kinase inhibitors p18(Ink4c) and p19(Ink4d).
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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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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.
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Who cites it
40 citing papers in PubMed, 122 citations in OpenAlex.
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- CIP/KIP and INK4 families as hostages of oncogenic signaling.Cell division · 2024Review
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- The Involvement of Ubiquitination Machinery in Cell Cycle Regulation and Cancer Progression.International journal of molecular sciences · 2021Review
- Bisphenol A-induced Alterations in Different Stages of Spermatogenesis and Systemic Toxicity in Albino Mice (Journal of health & pollution · 2021Article
- Sperm Functional Genome Associated With Bull Fertility.Frontiers in veterinary science · 2021Review
- The Role of CDKs and CDKIs in Murine Development.International journal of molecular sciences · 2020Review
- Two novel testis-specific long noncoding RNAs produced byThe Journal of reproduction and development · 2020Article
- Acute Damage to the Sperm Quality and Spermatogenesis in Male Mice Exposed to Curcumin-Loaded Nanoparticles.International journal of nanomedicine · 2020Article
- Diverse roles for CDK-associated activity during spermatogenesis.FEBS letters · 2019Review
- Germline deletion of Cdyl causes teratozoospermia and progressive infertility in male mice.Cell death & disease · 2019Article
- Genome-wide association for testis weight in the diversity outbred mouse population.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Interplay between p53 and Ink4c in spermatogenesis and fertility.Cell cycle (Georgetown, Tex.) · 2018Article
- Analyses of Long Non-Coding RNA and mRNA profiling using RNA sequencing in chicken testis with extreme sperm motility.Scientific reports · 2017Article
- Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice.Cell death & disease · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Male mice lacking both the Ink4c and Ink4d genes, which encode two inhibitors of D-type cyclin-dependent kinases (Cdks), are infertile, whereas female fecundity is unaffected. Both p18(Ink4c) and p19(Ink4d) are expressed in the seminiferous tubules of postnatal wild-type mice, being largely confined to postmitotic spermatocytes undergoing meiosis. Their combined loss is associated with the delayed exit of spermatogonia from the mitotic cell cycle, leading to the retarded appearance of meiotic cells that do not properly differentiate and instead undergo apoptosis at an increased frequency. As a result, mice lacking both Ink4c and Ink4d produce few mature sperm, and the residual spermatozoa have reduced motility and decreased viability. Whether or not Ink4d is present, animals lacking Ink4c develop hyperplasia of interstitial testicular Leydig cells, which produce reduced levels of testosterone. The anterior pituitary of fertile mice lacking Ink4c or infertile mice doubly deficient for Ink4c and Ink4d produces normal levels of luteinizing hormone (LH). Therefore, the failure of Leydig cells to produce testosterone is not secondary to defects in LH production, and reduced testosterone levels do not account for infertility in the doubly deficient strain. By contrast, Ink4d-null or double-null mice produce elevated levels of follicle-stimulating hormone (FSH). Because Ink4d-null mice are fertile, increased FSH production by the anterior pituitary is also unlikely to contribute to the sterility observed in Ink4c/Ink4d double-null males. Our data indicate that p18(Ink4c) and p19(Ink4d) are essential for male fertility. These two Cdk inhibitors collaborate in regulating spermatogenesis, helping to ensure mitotic exit and the normal meiotic maturation of spermatocytes.
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Registered trials
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