{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu J"],"funding":["NCI NIH HHS"],"pagination":["eadx8134"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12422196"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(37)"],"pubmed_abstract":["<i>PTDSS1</i> (phosphatidylserine synthase 1) encodes an enzyme that facilitates production of phosphatidylserine (PS), which mediates a global immunosuppressive signal. Here, based on in vivo CRISPR screen, we identified PTDSS1 as a target to improve anti-PD-1 therapy. Depletion of <i>Ptdss1</i> in tumor cells increased expression of interferon-γ (IFN-γ)-regulated genes, including <i>B2m</i>, <i>Cxcl9</i>, <i>Cxcl10</i>, and <i>Stat1</i>, even in the absence of IFN-γ stimulation in vitro. Loss of <i>Ptdss1</i> in tumor cells also led to increased expression of MHC-I, enhanced cytotoxicity of CD8<sup>+</sup> T cells, and increased frequency of an iNOS<sup>+</sup> myeloid subset. A gene signature derived from the iNOS<sup>+</sup> myeloid cell subset correlated with clinical benefit in patie"],"journal":["Science advances"],"pubmed_title":["Loss of PTDSS1 in tumor cells improves immunogenicity and response to anti-PD-1 therapy."],"pmcid":["PMC12422196"],"funding_grant_id":["P30 CA016672"],"pubmed_authors":["Nagarajan A","Goswami S","Liu J","Herbrich S","Xiong L","Sharma P","Anandhan S","Basu S","Chen Y","Guan B"],"additional_accession":[]},"is_claimable":false,"name":"Loss of PTDSS1 in tumor cells improves immunogenicity and response to anti-PD-1 therapy.","description":"<i>PTDSS1</i> (phosphatidylserine synthase 1) encodes an enzyme that facilitates production of phosphatidylserine (PS), which mediates a global immunosuppressive signal. Here, based on in vivo CRISPR screen, we identified PTDSS1 as a target to improve anti-PD-1 therapy. Depletion of <i>Ptdss1</i> in tumor cells increased expression of interferon-γ (IFN-γ)-regulated genes, including <i>B2m</i>, <i>Cxcl9</i>, <i>Cxcl10</i>, and <i>Stat1</i>, even in the absence of IFN-γ stimulation in vitro. Loss of <i>Ptdss1</i> in tumor cells also led to increased expression of MHC-I, enhanced cytotoxicity of CD8<sup>+</sup> T cells, and increased frequency of an iNOS<sup>+</sup> myeloid subset. A gene signature derived from the iNOS<sup>+</sup> myeloid cell subset correlated with clinical benefit in patie","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-02T20:21:55.043Z","creation":"2026-04-20T03:10:07.819Z"},"accession":"S-EPMC12422196","cross_references":{"pubmed":["40929270"],"doi":["10.1126/sciadv.adx8134"]}}