{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["O'Connor KW"],"funding":["NIAID NIH HHS","NHLBI NIH HHS","HHS | NIH | National Institute of Allergy and Infectious Diseases","NCI NIH HHS","Division of Intramural Research, National Institute of Allergy and Infectious Diseases"],"pagination":["e2220853120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10469339"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(35)"],"pubmed_abstract":["Ly6C<sup>lo</sup> monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6C<sup>lo</sup> monocytes have been shown to derive from Ly6C<sup>hi</sup> monocytes. NOTCH2 signaling has been implicated as a trigger for Ly6C<sup>lo</sup> monocyte development, but the basis for this effect is unclear. Here, we examined the impact of NOTCH2 signaling of myeloid progenitors on the development of Ly6C<sup>lo</sup> monocytes in vitro. NOTCH2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6C<sup>hi</sup> TREML4<sup>-</sup> monocytes into Ly6C<sup>lo</sup> TREML4<sup>+</sup> monocytes. We further identified two additional transcriptional requirements for development of Ly6C<sup>lo</sup> monocytes. Deletion of BCL6 from myel"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["<i>Bcl6</i>, <i>Irf2</i>, and <i>Notch2</i> promote nonclassical monocyte development."],"pmcid":["PMC10469339"],"funding_grant_id":["R01AI162643","R01 CA248919","R21 AI164142","R01 AI162643","R01 HL140622","R01AI150297","R01 AI150297"],"pubmed_authors":["Kim S","Georgopoulos K","Briseno CG","O'Connor KW","Murphy TL","Liu T","Murphy KM"],"additional_accession":[]},"is_claimable":false,"name":"<i>Bcl6</i>, <i>Irf2</i>, and <i>Notch2</i> promote nonclassical monocyte development.","description":"Ly6C<sup>lo</sup> monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6C<sup>lo</sup> monocytes have been shown to derive from Ly6C<sup>hi</sup> monocytes. NOTCH2 signaling has been implicated as a trigger for Ly6C<sup>lo</sup> monocyte development, but the basis for this effect is unclear. Here, we examined the impact of NOTCH2 signaling of myeloid progenitors on the development of Ly6C<sup>lo</sup> monocytes in vitro. NOTCH2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6C<sup>hi</sup> TREML4<sup>-</sup> monocytes into Ly6C<sup>lo</sup> TREML4<sup>+</sup> monocytes. We further identified two additional transcriptional requirements for development of Ly6C<sup>lo</sup> monocytes. Deletion of BCL6 from myel","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Aug","modification":"2025-04-18T13:13:44.816Z","creation":"2025-04-06T22:45:54.987Z"},"accession":"S-EPMC10469339","cross_references":{"pubmed":["37607223"],"doi":["10.1073/pnas.2220853120"]}}