{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Sijia Liang"],"species":["Homo Sapiens"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0017245000"],"submitter_email":["liangsj5@mail.sysu.edu.cn"],"submitter_affiliation":["Sun Yat-sen University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"additional_accession":[]},"is_claimable":false,"name":"Loss of ULK1 Promotes TLR4 Acetylation in THP-1 Macrophages","description":"This study focuses on the regulatory effect of ULK1 (Unc-51-like autophagy activating kinase 1) deficiency on TLR4 (Toll-like receptor 4) acetylation in THP-1 cells. ULK1, a key kinase involved in autophagy initiation, has been reported to participate in the regulation of various cellular processes, including inflammation and signal transduction. TLR4, a crucial pattern recognition receptor, plays a vital role in recognizing pathogen-associated molecular patterns and initiating innate immune responses, and its acetylation modification is closely related to the activation of downstream signaling pathways. In this study, ULK1-deficient THP-1 cells were constructed, and the acetylation level of TLR4 in the cells was detected by IP-MS methods. The results showed that the deficiency of ULK1 significantly promoted the acetylation of TLR4 in THP-1 cells, suggesting that ULK1 may act as a negative regulator of TLR4 acetylation.","dates":{"publication":"Thu Jun 04 00:00:00 BST 2026"},"accession":"PXD079259","cross_references":{"TAXONOMY":["9606"]}}