ArticlePloS one2014
The ubiquitin E3 ligase NOSIP modulates protein phosphatase 2A activity in craniofacial development.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- NOSIP promotes cell proliferation and motility by targeting SPTAN1 for ubiquitination and degradation in clear cell renal cell carcinoma.Scientific reports · 2026Article
- NOSIP overexpression promotes long-term persistence of CD8Frontiers in immunology · 2026Article
- Foxa1 disruption enhances human cell integration in human-mouse interspecies chimeras.Cell and tissue research · 2025Article
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- Article
- MicroRNA-124-3p suppresses mouse lip mesenchymal cell proliferation through the regulation of genes associated with cleft lip in the mouse.BMC genomics · 2019Article
- Control of mTOR signaling by ubiquitin.Oncogene · 2019Review
- Differential DNA methylation at birth associated with mental disorder in individuals with 22q11.2 deletion syndrome.Translational psychiatry · 2017Article
- FAM122A, a new endogenous inhibitor of protein phosphatase 2A.Oncotarget · 2016Article
- The eNOS signalosome and its link to endothelial dysfunction.Pflugers Archiv : European journal of physiology · 2016Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Holoprosencephaly is a common developmental disorder in humans characterised by incomplete brain hemisphere separation and midface anomalies. The etiology of holoprosencephaly is heterogeneous with environmental and genetic causes, but for a majority of holoprosencephaly cases the genes associated with the pathogenesis could not be identified so far. Here we report the generation of knockout mice for the ubiquitin E3 ligase NOSIP. The loss of NOSIP in mice causes holoprosencephaly and facial anomalies including cleft lip/palate, cyclopia and facial midline clefting. By a mass spectrometry based protein interaction screen we identified NOSIP as a novel interaction partner of protein phosphatase PP2A. NOSIP mediates the monoubiquitination of the PP2A catalytic subunit and the loss of NOSIP results in an increase in PP2A activity in craniofacial tissue in NOSIP knockout mice. We conclude, that NOSIP is a critical modulator of brain and craniofacial development in mice and a candidate gene for holoprosencephaly in humans.
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