{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kataru RP"],"funding":["Emerson Collective Cancer Research Fund","NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS","National Institutes of Health","NIAMS NIH HHS"],"pagination":["eabc0836"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8567054"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(695)"],"pubmed_abstract":["Exogenous administration of lymphangiogenic growth factors is widely used to study changes in lymphatic function in pathophysiology. However, this approach can result in off-target effects, thereby generating conflicting data. To circumvent this issue, we modulated intracellular VEGF-C signaling by conditionally knocking out the lipid phosphatase PTEN using the <i>Vegfr3</i> promoter to drive the expression of <i>Cre-lox</i> in lymphatic endothelial cells (LECs). PTEN is an intracellular brake that inhibits the downstream effects of the activation of VEGFR3 by VEGF-C. Activation of Cre-lox recombination in adult mice resulted in an expanded functional lymphatic network due to LEC proliferation that was independent of lymphangiogenic growth factor production. Furthermore, compared with lymp"],"journal":["Science signaling"],"pubmed_title":["Lymphatic-specific intracellular modulation of receptor tyrosine kinase signaling improves lymphatic growth and function."],"pmcid":["PMC8567054"],"funding_grant_id":["T32 CA009501","HL111130","R01 HL111130","P30 CA008748","R01 AI079178","T32 AR071302","691032"],"pubmed_authors":["Baik JE","Lu TT","Ortega S","Park HJ","Shin J","Ly CL","Mehrara BJ","Kataru RP","Schwartz N"],"additional_accession":[]},"is_claimable":false,"name":"Lymphatic-specific intracellular modulation of receptor tyrosine kinase signaling improves lymphatic growth and function.","description":"Exogenous administration of lymphangiogenic growth factors is widely used to study changes in lymphatic function in pathophysiology. However, this approach can result in off-target effects, thereby generating conflicting data. To circumvent this issue, we modulated intracellular VEGF-C signaling by conditionally knocking out the lipid phosphatase PTEN using the <i>Vegfr3</i> promoter to drive the expression of <i>Cre-lox</i> in lymphatic endothelial cells (LECs). PTEN is an intracellular brake that inhibits the downstream effects of the activation of VEGFR3 by VEGF-C. Activation of Cre-lox recombination in adult mice resulted in an expanded functional lymphatic network due to LEC proliferation that was independent of lymphangiogenic growth factor production. Furthermore, compared with lymp","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2025-04-22T22:04:07.405Z","creation":"2025-04-06T03:54:03.714Z"},"accession":"S-EPMC8567054","cross_references":{"pubmed":["34376570"],"doi":["10.1126/scisignal.abc0836"]}}