ABSTRACT: We investigated SOX18 binding events on the chromatin under basal conditions in human umbilical vein endothelial cells, upon overexpression of mouse Sox18-cMyc and immunoprecipitating cMyc. Cells overexpressing only the cMyc tag were used as negative control condition, and peaks called here were substracted from the Sox18-cMyc peaks.
Project description:We investigated SOX7 binding events on the chromatin under basal conditions in human umbilical vein endothelial cells, upon overexpression of human SOX7-mCherry and immunoprecipitating mCherry. Cells overexpressing only the mCherry tag were used as negative control condition, and peaks called here were substracted from the SOX7-mCherry peaks.
Project description:We investigated the transcriptome of HUVECs under basal conditions and overexpression of Sox18 in presence or absence of small molecule protein-protein disruptor Sm4. Various RNA fractions were prepared and sequenced in order to characterise Sox18 and Sm4 responsive genes in HUVECs
Project description:We investigated differences in the chromatin-binding profile of SOX18 (mouse) and its dominant-negative isoform SOX18RaOp, and how SOX18RaOp alters the binding location of SOX18. HeLa cells were transfected to generate 3 different conditions: 1. myc-SOX18, 2. myc-SOX18RaOp and 3. myc-SOX18 with untagged-SOX18RaOp. Each condition was performed in duplicate (6 samples total). An anti-Myc antibody was used to perform the pull-down. Background (input) was assessed by pooling cells transfected with each condition and sequencing without immunoprecipitation.
Project description:Study of Sox18 regulated genes: Human umbilical vein endothelial cells (HUVEC) were either transduced with adenoviral vectors expressing SOX18 from an IRES-EGFP casette, or IRES-EGFP alone, or left untreated. After 16 hours, mRNA was isolated and analyzed by hybridization to Affymetrix HG-U133A arrays.
Project description:Study of Sox18 regulated genes: Human umbilical vein endothelial cells (HUVEC) were either transduced with adenoviral vectors expressing SOX18 from an IRES-EGFP casette, or IRES-EGFP alone, or left untreated. After 16 hours, mRNA was isolated and analyzed by hybridization to Affymetrix HG-U133A arrays. Human umbilical vein endothelial cells (HUVEC) were either transduced with adenoviral vectors expressing SOX18 from an IRES-EGFP casette, or IRES-EGFP alone, or left untreated. After 16 hours, mRNA was isolated and analyzed by hybridization to Affymetrix HG-U133A arrays.
Project description:Using inducible SOX18 human PSCs, we found overexpression of SOX18 showed change of transcriptional program at D8 especially T cell receptor and Toll like receptor signaling pathways. So this suggests SOX18 has an effect on lymphoid differentiation program. Specifically overexpressed SOX18 enhance NK cell production, and related to metabolism pathway. This finding that SOX18 promotes development of progenitors with superior NK cell potenital will advance our understanding of molecualr network regulating specification on lymphoid cells and can help to improve the scalability of NK CELL production form hPSCs form immunotherapies.
Project description:We intended to identify the potential binding sites of Sox18 Ragged transcription factor in the zebrafish during development (26-28hpf).
Project description:Infantile hemangioma (IH) is the most common tumor in children and a paradigm for pathological vasculogenesis, angiogenesis and regression. Propranolol is the mainstay of treatment for IH. It inhibits hemangioma vessel formation via a β-adrenergic receptor independent effect of its R(+) enantiomer on the endothelial specific transcription factor sex-determining region Y (SRY) box transcription factor 18 (SOX18). Transcriptomic profiling of patient-derived hemangioma stem cells uncovered the mevalonate pathway (MVP) as a target of R(+) propranolol. Loss of SOX18 function confirmed R(+) propranolol mode of action on the MVP. Functional validation in preclinical IH models revealed that statins - targeting the MVP - are potent inhibitors of hemangioma vessel formation. We propose a novel SOX18-MVP-axis as a central regulator of IH pathogenesis and suggest statin repurposing to treat IH.
Project description:Infantile hemangioma (IH) is the most common tumor in children and a paradigm for pathological vasculogenesis, angiogenesis and regression. Propranolol is the mainstay of treatment for IH. It inhibits hemangioma vessel formation via a β-adrenergic receptor independent effect of its R(+) enantiomer on the endothelial specific transcription factor sex-determining region Y (SRY) box transcription factor 18 (SOX18). Transcriptomic profiling of patient-derived hemangioma stem cells uncovered the mevalonate pathway (MVP) as a target of R(+) propranolol. Loss of SOX18 function confirmed R(+) propranolol mode of action on the MVP. Functional validation in preclinical IH models revealed that statins - targeting the MVP - are potent inhibitors of hemangioma vessel formation. We propose a novel SOX18-MVP-axis as a central regulator of IH pathogenesis and suggest statin repurposing to treat IH.