ArticleHuman molecular genetics2020
A mouse model for kinesin family member 11 (Kif11)-associated familial exudative vitreoretinopathy.
Article in Human molecular genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Traffic Jams in the Brain: How Kinesin Dysfunction Shapes Neurodevelopmental Disorders.Current issues in molecular biology · 2026Review
- Choroidal imaging features of KIF11-associated retinopathy: expanding the ocular phenotype.International journal of retina and vitreous · 2026Article
- Computational Quantification of Mouse Retinal Vasculature Using ImageJ.Bio-protocol · 2026Article
- KIF11 prevents retinal endothelial ferroptosis in familial exudative vitreoretinopathy by inhibiting phosphorylation-driven PRDX1 phase separation.Nature communications · 2026Article
- Intellectual disability-causing mutations in KIF11 impair microtubule dynamics and dendritic arborization.Nature communications · 2026Article
- Insights into KIF11 pathogenesis in microcephaly-lymphedema-chorioretinopathy syndrome from a lymphatic perspective.JCI insight · 2026Article
- KIF11 variants in familial exudative vitreoretinopathy leading to mTORC1 overactivation and impaired cell cycle progression.Human genomics · 2025Article
- Microcephaly with or without chorioretinopathy, lymphedema, or mental retardation associated with KIF11 pathogenic variant: case report and genotype-phenotype correlation analysis.BMC ophthalmology · 2025Article
- The MDM2-p53 axis regulates norrin/frizzled4 signaling and blood-CNS barrier function.Science signaling · 2025Article
- Identification and validation of the important role of KIF11 in the development and progression of endometrial cancer.Journal of translational medicine · 2025Article
- Characteristics of blood-brain barrier heterogeneity between brain regions revealed by profiling vascular and perivascular cells.Nature neuroscience · 2024Article
- PMEcotoxicology and environmental safety · 2024Article
- Eg5 and Diseases: From the Well-Known Role in Cancer to the Less-Known Activity in Noncancerous Pathological Conditions.Biochemistry research international · 2024Review
- Review
- Defective EMC1 drives abnormal retinal angiogenesis via Wnt/β-catenin signaling and may be associated with the pathogenesis of familial exudative vitreoretinopathy.Genes & diseases · 2023Article
- Loss of Tbx3 in Mouse Eye Causes Retinal Angiogenesis Defects Reminiscent of Human Disease.Investigative ophthalmology & visual science · 2023Article
- Cellular and Molecular Mechanisms of Pathogenesis Underlying Inherited Retinal Dystrophies.Biomolecules · 2023Review
- Kinesin-5 Eg5 is essential for spindle assembly, chromosome stability and organogenesis in development.Cell death discovery · 2022Article
- KIF11: A potential prognostic biomarker for predicting bone metastasis-free survival of prostate cancer.Oncology letters · 2022Article
- CTNND1 variants cause familial exudative vitreoretinopathy through the Wnt/cadherin axis.JCI insight · 2022Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
During mitosis, Kif11, a kinesin motor protein, promotes bipolar spindle formation and chromosome movement, and during interphase, Kif11 mediates diverse trafficking processes in the cytoplasm. In humans, inactivating mutations in KIF11 are associated with (1) retinal hypovascularization with or without microcephaly and (2) multi-organ syndromes characterized by variable combinations of lymphedema, chorioretinal dysplasia, microcephaly and/or mental retardation. To explore the pathogenic basis of KIF11-associated retinal vascular disease, we generated a Kif11 conditional knockout (CKO) mouse and investigated the consequences of early postnatal inactivation of Kif11 in vascular endothelial cells (ECs). The principal finding is that postnatal EC-specific loss of Kif11 leads to severely stunted growth of the retinal vasculature, mildly stunted growth of the cerebellar vasculature and little or no effect on the vasculature elsewhere in the central nervous system (CNS). Thus, in mice, Kif11 function in early postnatal CNS ECs is most significant in the two CNS regions-the retina and cerebellum-that exhibit the most rapid rate of postnatal growth, which may sensitize ECs to impaired mitotic spindle function. Several lines of evidence indicate that these phenotypes are not caused by reduced beta-catenin signaling in ECs, despite the close resemblance of the Kif11 CKO phenotype to that caused by EC-specific reductions in beta-catenin signaling. Based on prior work, defective beta-catenin signaling had been the only known mechanism responsible for monogenic human disorders of retinal hypovascularization. The present study implies that retinal hypovascularization can arise from a second and mechanistically distinct cause.
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