{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kwak EA"],"funding":["U.S. Department of Health &amp; Human Services | NIH | National Institute of General Medical Sciences","NIDA NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["1326"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8921520"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Defective angiogenesis underlies over 50 malignant, ischemic and inflammatory disorders yet long-term therapeutic applications inevitably fail, thus highlighting the need for greater understanding of the vast crosstalk and compensatory mechanisms. Based on proteomic profiling of angiogenic endothelial components, here we report β<sub>IV</sub>-spectrin, a non-erythrocytic cytoskeletal protein, as a critical regulator of sprouting angiogenesis. Early loss of endothelial-specific β<sub>IV</sub>-spectrin promotes embryonic lethality in mice due to hypervascularization and hemorrhagic defects whereas neonatal depletion yields higher vascular density and tip cell populations in developing retina. During sprouting, β<sub>IV</sub>-spectrin expresses in stalk cells to inhibit their tip cell potenti"],"journal":["Nature communications"],"pubmed_title":["β<sub>IV</sub>-spectrin as a stalk cell-intrinsic regulator of VEGF signaling."],"pmcid":["PMC8921520"],"funding_grant_id":["P30 DA051355","GM128055","P30 CA023074","R01 CA219495","R01 GM128055"],"pubmed_authors":["Lee YS","Largent-Milnes T","Ahmed T","Cruz-Flores P","Vanderah TW","Langlais PR","Mohler PJ","Kwak EA","Ramonett A","Lochhead JJ","Pan CC","Kumar S","Hund TJ","Lee NY","Mouneimne G","Mythreye K","Georgieva TG","Ortiz HR","Ellis NA"],"additional_accession":[]},"is_claimable":false,"name":"β<sub>IV</sub>-spectrin as a stalk cell-intrinsic regulator of VEGF signaling.","description":"Defective angiogenesis underlies over 50 malignant, ischemic and inflammatory disorders yet long-term therapeutic applications inevitably fail, thus highlighting the need for greater understanding of the vast crosstalk and compensatory mechanisms. Based on proteomic profiling of angiogenic endothelial components, here we report β<sub>IV</sub>-spectrin, a non-erythrocytic cytoskeletal protein, as a critical regulator of sprouting angiogenesis. Early loss of endothelial-specific β<sub>IV</sub>-spectrin promotes embryonic lethality in mice due to hypervascularization and hemorrhagic defects whereas neonatal depletion yields higher vascular density and tip cell populations in developing retina. During sprouting, β<sub>IV</sub>-spectrin expresses in stalk cells to inhibit their tip cell potenti","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2025-04-04T13:18:34.097Z","creation":"2025-04-04T13:18:34.097Z"},"accession":"S-EPMC8921520","cross_references":{"pubmed":["35288568"],"doi":["10.1038/s41467-022-28933-1"]}}