ArticleMolecular and cellular biology2002
Developmental defects and male sterility in mice lacking the ubiquitin-like DNA repair gene mHR23B.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 107 citations in OpenAlex.
- Review
- Is Male Infertility an Early Warning of More Serious Diseases?Endocrinology · 2026Review
- Article
- PFOA-Induced Ovotoxicity Differs Between Lean and Obese Mice With Impacts on Ovarian Reproductive and DNA Damage Sensing and Repair Proteins.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Destruction or Reconstruction: A Subtle Liaison between the Proteolytic and Signaling Role of Protein Ubiquitination in Spermatogenesis.Advances in experimental medicine and biology · 2021Article
- Comparative distributions of RSBN1 and methylated histone H4 Lysine 20 in the mouse spermatogenesis.PloS one · 2021Article
- Multi-Step Ubiquitin Decoding Mechanism for Proteasomal Degradation.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Nucleotide excision repair genes shaping embryonic development.Open biology · 2019Review
- Inadequate ubiquitination-proteasome coupling contributes to myocardial ischemia-reperfusion injury.The Journal of clinical investigation · 2018Article
- C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.Nature neuroscience · 2016Article
- Molecular basis of cleft palates in mice.World journal of biological chemistry · 2015Review
- Functional and mechanistic studies of XPC DNA-repair complex as transcriptional coactivator in embryonic stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Erythropoietic defect associated with reduced cell proliferation in mice lacking the 26S proteasome shuttling factor Rad23b.Molecular and cellular biology · 2013Article
- Article
- The REV7 subunit of DNA polymerase ζ is essential for primordial germ cell maintenance in the mouse.The Journal of biological chemistry · 2013Article
- Why do cellular proteins linked to K63-polyubiquitin chains not associate with proteasomes?The EMBO journal · 2013Article
- Age-related neuronal degeneration: complementary roles of nucleotide excision repair and transcription-coupled repair in preventing neuropathology.PLoS genetics · 2011Article
- Fine-mapping alleles for body weight in LG/J × SM/J F₂ and F(34) advanced intercross lines.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Article
- Mouse Rad9b is essential for embryonic development and promotes resistance to DNA damage.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Article
- Ubiquitin-binding domains - from structures to functions.Nature reviews. Molecular cell biology · 2009Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 5 countries.
Funding
Abstract
mHR23B encodes one of the two mammalian homologs of Saccharomyces cerevisiae RAD23, a ubiquitin-like fusion protein involved in nucleotide excision repair (NER). Part of mHR23B is complexed with the XPC protein, and this heterodimer functions as the main damage detector and initiator of global genome NER. While XPC defects exist in humans and mice, mutations for mHR23A and mHR23B are not known. Here, we present a mouse model for mHR23B. Unlike XPC-deficient cells, mHR23B(-/-) mouse embryonic fibroblasts are not UV sensitive and retain the repair characteristics of wild-type cells. In agreement with the results of in vitro repair studies, this indicates that mHR23A can functionally replace mHR23B in NER. Unexpectedly, mHR23B(-/-) mice show impaired embryonic development and a high rate (90%) of intrauterine or neonatal death. Surviving animals display a variety of abnormalities, including retarded growth, facial dysmorphology, and male sterility. Such abnormalities are not observed in XPC and other NER-deficient mouse mutants and point to a separate function of mHR23B in development. This function may involve regulation of protein stability via the ubiquitin/proteasome pathway and is not or only in part compensated for by mHR23A.
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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.