<HashMap><database>iProX</database><scores/><additional><omics_type>Proteomics</omics_type><submitter>Sijia Liang</submitter><species>Homo Sapiens</species><full_dataset_link>http://www.iprox.org/page/project.html?id=IPX0017245000</full_dataset_link><submitter_email>liangsj5@mail.sysu.edu.cn</submitter_email><submitter_affiliation>Sun Yat-sen University</submitter_affiliation><sample_protocol></sample_protocol><repository>iProX</repository><data_protocol></data_protocol></additional><is_claimable>false</is_claimable><name>Loss of ULK1 Promotes TLR4 Acetylation in THP-1 Macrophages</name><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.</description><dates><publication>Thu Jun 04 00:00:00 BST 2026</publication></dates><accession>PXD079259</accession><cross_references><TAXONOMY>9606</TAXONOMY></cross_references></HashMap>