{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dai Y"],"funding":["Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation)","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["33"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12804790"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(1)"],"pubmed_abstract":["Endogenous nitric oxide (NO) produced by nitric oxide synthases (NOSs) plays an important immunosuppressive role in the tumor microenvironment. In melanoma, NOS1 expression increases with tumor progression and correlates with tumor immune escape through the inhibition of type I interferon (IFN) signaling. However, the immune regulatory role and related mechanisms of NOS1, as well as its impacts on immune therapies such as immune checkpoint blockade (ICB) in melanoma, remain unclear. Here, we found that NOS1 expression induces IRF7 modification by S-nitrosylation at the C435 site in mice (C481 in humans), which functionally promoted tumor growth in mouse models. Mechanistically, IRF7-C435-SNO inhibited IFNβ transcription under PRR signal activation, leading to a disorder in the initiation o"],"journal":["Cell death & disease"],"pubmed_title":["S-nitrosylation of IRF7 induced by NOS1 expression in melanoma suppresses anti-tumor immunity."],"pmcid":["PMC12804790"],"funding_grant_id":["2021YFC2009100，2021YFC2009105","82073143"],"pubmed_authors":["Zeng S","Yuan S","Huang J","Chen J","Liu N","Yang M","Huang M","Liu Q","Guo S","Li K","Zhong Z","Dai Y","Wang Q","Ye S","Zhu L","Gao W","Chen X","Hao B"],"additional_accession":[]},"is_claimable":false,"name":"S-nitrosylation of IRF7 induced by NOS1 expression in melanoma suppresses anti-tumor immunity.","description":"Endogenous nitric oxide (NO) produced by nitric oxide synthases (NOSs) plays an important immunosuppressive role in the tumor microenvironment. In melanoma, NOS1 expression increases with tumor progression and correlates with tumor immune escape through the inhibition of type I interferon (IFN) signaling. However, the immune regulatory role and related mechanisms of NOS1, as well as its impacts on immune therapies such as immune checkpoint blockade (ICB) in melanoma, remain unclear. Here, we found that NOS1 expression induces IRF7 modification by S-nitrosylation at the C435 site in mice (C481 in humans), which functionally promoted tumor growth in mouse models. Mechanistically, IRF7-C435-SNO inhibited IFNβ transcription under PRR signal activation, leading to a disorder in the initiation o","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-12T05:00:49.892Z","creation":"2026-06-12T03:07:53.619Z"},"accession":"S-EPMC12804790","cross_references":{"pubmed":["41535256"],"doi":["10.1038/s41419-025-08201-y"]}}