ArticleReproductive biology and endocrinology : RB&E2007
Ubp43 gene expression is required for normal Isg15 expression and fetal development.
Article in Reproductive biology and endocrinology : RB&E, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Protein ISGylation: a posttranslational modification with implications for malignant neoplasms.Exploration of targeted anti-tumor therapy · 2023Review
- The diverse repertoire of ISG15: more intricate than initially thought.Experimental & molecular medicine · 2022Review
- RIG-I regulates myeloid differentiation by promoting TRIM25-mediated ISGylation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Multiple functions of USP18.Cell death & disease · 2016Review
- Evidence for the ubiquitin protease UBP43 as an antineoplastic target.Molecular cancer therapeutics · 2012Article
- Gene expression profiling in the submandibular gland, stomach, and duodenum of CAVI-deficient mice.Transgenic research · 2011Article
- Blockade of the ubiquitin protease UBP43 destabilizes transcription factor PML/RARα and inhibits the growth of acute promyelocytic leukemia.Cancer research · 2010Article
- Do molecular signals from the conceptus influence endometrium decidualization in rodents?Journal of experimental zoology. Part B, Molecular and developmental evolution · 2009Review
- Epstein-Barr virus independent dysregulation of UBP43 expression alters interferon-stimulated gene expression in Burkitt lymphoma.PloS one · 2009Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundIsg15 covalently modifies murine endometrial proteins in response to early pregnancy. Isg15 can also be severed from targeted proteins by a specific protease called Ubp43 (Usp18). Mice lacking Ubp43 (null) form increased conjugated Isg15 in response to interferon. The Isg15 system has not been examined in chorioallantoic placenta (CP) or mesometrial (MM) components of implantation sites beyond 9.5 days post coitum (dpc). It was hypothesized that deletion of Ubp43 would cause disregulation of Isg15 in implantation sites, and that this would affect pregnancy rates.
methodsHeterozygous (het) Ubp43 mice were mated and MM and CP implantation sites were collected on 12.5 and 17.5 days post-coitum (dpc).
resultsFree and conjugated Isg15 were greater on 12.5 versus 17.5 dpc in MM. Free and conjugated Isg15 were also present in CP, but did not differ due to genotype on 12.5 dpc. However, null CP had greater free and conjugated Isg15 when compared to het/wt on 17.5 dpc. Null progeny died in utero with fetal genotype ratios (wt:het:null) of 2:5:1 on 12.5 and 2:2:1 on 17.5 dpc. Implantation sites were disrupted within the junctional zone and spongiotrophoblast, contained less vasculature based on lectin B4 staining and contained greater Isg15 mRNA and VEGF protein in Ubp43 null when compared to wt placenta.
conclusionIt is concluded that Isg15 and its conjugates are present in implantation sites during mid to late gestation and that deletion of Ubp43 causes an increase in free and conjugated Isg15 at the feto-maternal interface. Also, under mixed genetic background, deletion of Ubp43 results in fetal death.
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