ArticleMolecular and cellular biology2003
Female lethality and apoptosis of spermatocytes in mice lacking the UBR2 ubiquitin ligase of the N-end rule pathway.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 150 citations in OpenAlex.
- The Potential Role of Deubiquitinating Enzymes (DUBs) in Male Fertility.Biomolecules · 2026Review
- The role of UBR2 in triple-negative breast cancer and its implications for immune checkpoint blockade therapy.Discover oncology · 2025Article
- An essential role of the E3 ubiquitin ligase RNF126 in ensuring meiosis I completion during spermatogenesis.Journal of advanced research · 2025Article
- SOD2 is a regulator of proteasomal degradation promoting an adaptive cellular starvation response.Cell reports · 2025Article
- The phosphatase DUSP22 inhibits UBR2-mediated K63-ubiquitination and activation of Lck downstream of TCR signalling.Nature communications · 2024Article
- Metabolic regulation of proteome stability via N-terminal acetylation controls male germline stem cell differentiation and reproduction.Nature communications · 2023Article
- Research progress on exosomal proteins as diagnostic markers of gastric cancer (review article).Clinical and experimental medicine · 2023Review
- Iron-sulfur clusters are involved in post-translational arginylation.Nature communications · 2023Article
- UBR2 targets myosin heavy chain IIb and IIx for degradation: Molecular mechanism essential for cancer-induced muscle wasting.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Meiotic DNA breaks activate a streamlined phospho-signaling response that largely avoids protein-level changes.Life science alliance · 2022Article
- Review
- The Conceivable Functions of Protein Ubiquitination and Deubiquitination in Reproduction.Frontiers in physiology · 2022Review
- Proteolysis in Reproduction: Lessons From Gene-Modified Organism Studies.Frontiers in endocrinology · 2022Review
- E3 ubiquitin ligase ASB17 is required for spermiation in mice.Translational andrology and urology · 2021Article
- The E3 ligase UBR2 regulates cell death under caspase deficiency via Erk/MAPK pathway.Cell death & disease · 2020Article
- The ATF3 Transcription Factor Is a Short-Lived Substrate of the Arg/N-Degron Pathway.Biochemistry · 2020Article
- Tex19.1 inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes.The Journal of cell biology · 2020Article
- Downregulation of the Arg/N-degron Pathway Sensitizes Cancer Cells to Chemotherapy In Vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Structural Analyses on the Deamidation of N-Terminal Asn in the Human N-Degron Pathway.Biomolecules · 2020Article
- Screening of targeted panel genes in Brazilian patients with primary ovarian insufficiency.PloS one · 2020Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Substrates of the ubiquitin-dependent N-end rule pathway include proteins with destabilizing N-terminal residues. UBR1(-/-) mice, which lacked the pathway's ubiquitin ligase E3alpha, were viable and retained the N-end rule pathway. The present work describes the identification and analysis of mouse UBR2, a homolog of UBR1. We demonstrate that the substrate-binding properties of UBR2 are highly similar to those of UBR1, identifying UBR2 as the second E3 of the mammalian N-end rule pathway. UBR2(-/-) mouse strains were constructed, and their viability was found to be dependent on both gender and genetic background. In the strain 129 (inbred) background, the UBR2(-/-) genotype was lethal to most embryos of either gender. In the 129/B6 (mixed) background, most UBR2(-/-) females died as embryos, whereas UBR2(-/-) males were viable but infertile, owing to the postnatal degeneration of the testes. The gross architecture of UBR2(-/-) testes was normal and spermatogonia were intact as well, but UBR2(-/-) spermatocytes were arrested between leptotene/zygotene and pachytene and died through apoptosis. A conspicuous defect of UBR2(-/-) spermatocytes was the absence of intact synaptonemal complexes. We conclude that the UBR2 ubiquitin ligase and, hence, the N-end rule pathway are required for male meiosis and spermatogenesis and for an essential aspect of female embryonic development.
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