ArticlePloS one2015
ANKS1B Interacts with the Cerebral Cavernous Malformation Protein-1 and Controls Endothelial Permeability but Not Sprouting Angiogenesis.
Article in PloS one, 2015. 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, 13 citations in OpenAlex.
- Cerebral Cavernous Malformation (CCM)-like Vessel Lesion in the AgedExperimental neurobiology · 2023Article
- Transcriptome analysis of cervical cancer exosomes and detection of HPVE6*I transcripts in exosomal RNA.BMC cancer · 2022Article
- Mechanistic characterization of endothelial sprouting mediated by pro-angiogenic signaling.Microcirculation (New York, N.Y. : 1994) · 2022Article
- Integrated analysis of Shank1 PDZ interactions with C-terminal and internal binding motifs.Current research in structural biology · 2021Article
- Short-term treatment with dabigatran alters protein expression patterns in a late-stage tau-based Alzheimer's disease mouse model.Biochemistry and biophysics reports · 2020Article
- Screening of key genes associated with R‑CHOP immunochemotherapy and construction of a prognostic risk model in diffuse large B‑cell lymphoma.Molecular medicine reports · 2019Article
- Recent advances in cerebral cavernous malformation research.Vessel plus · 2018Article
- Novel functions of CCM1 delimit the relationship of PTB/PH domains.Biochimica et biophysica acta. Proteins and proteomics · 2017Article
- Niche harmony search algorithm for detecting complex disease associated high-order SNP combinations.Scientific reports · 2017Article
- HIF-1α and HIF-2α induced angiogenesis in gastrointestinal vascular malformation and reversed by thalidomide.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral cavernous malformations are fragile blood vessel conglomerates in the central nervous system that are caused by mutations in the CCM1/KRIT1, CCM2 or CCM3 genes. The gene products form a protein complex at adherens junctions and loss of either CCM protein disrupts endothelial cell quiescence leading to increased permeability and excessive angiogenesis. We performed a yeast 2-hybrid screen to identify novel proteins directly interacting with KRIT1. The ankyrin repeat and sterile alpha motif domain-containing protein 1B (ANKS1B) was identified as a novel binding partner of KRIT1. Silencing of ANKS1B or the related gene ANKS1A in primary human endothelial cells had no significant effects on cellular proliferation, migration and sprouting angiogenesis. However, silencing of ANKS1B expression disturbed endothelial cell barrier functions leading to increased permeability. Forced ANKS1B expression reduced permeability. This was independent of Rho kinase activity and the presence of KRIT1. Taken together, ANKS1B was identified as a novel KRIT1-interacting protein that selectively controls endothelial permeability but not angiogenesis.
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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.