In endothelial cells, USP10 interacts with and stabilizes the NOTCH1 intracellular domain (NICD1), slowing its ubiquitin-dependent turnover. Endothelial-specific deletion of Usp10 (via Pdgfb‑creERT2 in Usp10^fl/fl) increases vessel sprouting and tip-cell formation in postnatal mouse retina, phenocopying reduced Notch signaling; USP10 loss partially rescues ectopic NICD1 overexpression vascular defects repisalud.isciii.es+14pubmed.ncbi.nlm.nih.gov+14researchgate.net+14
Endothelial deletion of Usp10 destabilizes NICD1, reduces canonical Notch target activation; increases EC density and filopodia in retinal angiogenesis; rescues NICD1‑overexpression vascular anomalies
Pdgfb‑creERT2; Usp10^fl/fl endothelial-specific, inducible knockout (genOway-generated, C57BL/6)
Vascular morphogenesis; angiogenic sprouting; endothelial Notch signaling; ocular vascular development; tip/stalk cell patterning
Conditional floxed allele (exons 7‑8 flanked by loxP); inducible CreERT2 under Pdgfb promoter; tamoxifen dosing P1–P4; retinal angiogenesis assay at P7; germline KO lethal
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