ArticleThe American journal of pathology2003
Expression of a K48R mutant ubiquitin protects mouse testis from cryptorchid injury and aging.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Expression of Protein Markers in Spermatogenic and Supporting Sertoli Cells Affected by High Abdominal Temperature in Cryptorchidism Model Mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation.Respiratory research · 2018Article
- Article
- Possible role of ZPAC, zygote-specific proteasome assembly chaperone, during spermatogenesis in the mouse.The Journal of reproduction and development · 2014Article
- Localization of ubiquitin C-terminal hydrolase L1 in mouse ova and its function in the plasma membrane to block polyspermy.The American journal of pathology · 2006Article
- Delayed testicular aging in pituitary adenylate cyclase-activating peptide (PACAP) null mice.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Two closely related ubiquitin C-terminal hydrolase isozymes function as reciprocal modulators of germ cell apoptosis in cryptorchid testis.The American journal of pathology · 2004Article
- Male reprotoxicity and endocrine disruption.Experientia supplementum (2012)Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Testis injury models can be useful for determining the in vivo function of genes. In this study, ubiquitin, a tag for 26S-proteasome degradation, was mutated at lysine 48 (K48R) to inhibit ubiquitin chain assembly. K48R transgenic mice had testes with delayed germ cell loss following the acute injury of experimental cryptorchidism, and were resistant to the chronic injury of aging-associated testicular atrophy. After 4 days of cryptorchid-mediated heat stress, the average weight of cryptorchid testes in wild-type ubiquitin mice was significantly lower (P < 0.05) than in K48R mutant ubiquitin mice, indicating that altered ubiquitination delayed germ cell death. Light microscopy confirmed that the testicular injury, in both wild-type and K48R ubiquitin mice, was due to germ cell death. In addition, wild-type ubiquitin mice aged 19 to 22 months showed greater testicular atrophy and decreased average seminiferous tubule diameter when compared with K48R-aged testes. These results demonstrate a resistance to testicular injury conferred by the K48R mutation, suggesting that ubiquitin-mediated protein degradation is involved in the processing or modulation of testicular insults.
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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.