{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["44(9)"],"submitter":["Guedes JP"],"pubmed_abstract":["N-terminal acetyltransferase B (NatB) is a major contributor to the N-terminal acetylome and is implicated in several key cellular processes including apoptosis and proteostasis. However, the molecular mechanisms linking NatB-mediated N-terminal acetylation to apoptosis and its relationship with protein homeostasis remain elusive. In this study, we generated mouse embryonic fibroblasts (MEFs) with an inactivated catalytic subunit of NatB (<i>Naa20</i><sup>-/-</sup>) to investigate the impact of NatB deficiency on apoptosis regulation. Through quantitative N-terminomics, label-free quantification, and targeted proteomics, we demonstrated that NatB does not influence the proteostasis of all its substrates. Instead, our focus on putative NatB-dependent apoptotic factors revealed that NatB ser"],"journal":["Molecular and cellular biology"],"pagination":["358-371"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11376409"],"repository":["biostudies-literature"],"pubmed_title":["NatB Protects Procaspase-8 from UBR4-Mediated Degradation and Is Required for Full Induction of the Extrinsic Apoptosis Pathway."],"pmcid":["PMC11376409"],"pubmed_authors":["Boyer JB","Meinnel T","Giglione C","Carte B","Redeker V","Corte-Real M","Guedes JP","Sago L","Aldabe R","Elurbide J"],"additional_accession":[]},"is_claimable":false,"name":"NatB Protects Procaspase-8 from UBR4-Mediated Degradation and Is Required for Full Induction of the Extrinsic Apoptosis Pathway.","description":"N-terminal acetyltransferase B (NatB) is a major contributor to the N-terminal acetylome and is implicated in several key cellular processes including apoptosis and proteostasis. However, the molecular mechanisms linking NatB-mediated N-terminal acetylation to apoptosis and its relationship with protein homeostasis remain elusive. In this study, we generated mouse embryonic fibroblasts (MEFs) with an inactivated catalytic subunit of NatB (<i>Naa20</i><sup>-/-</sup>) to investigate the impact of NatB deficiency on apoptosis regulation. Through quantitative N-terminomics, label-free quantification, and targeted proteomics, we demonstrated that NatB does not influence the proteostasis of all its substrates. Instead, our focus on putative NatB-dependent apoptotic factors revealed that NatB ser","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2026-03-27T15:56:36.483Z","creation":"2025-08-30T03:06:09.334Z"},"accession":"S-EPMC11376409","cross_references":{"pubmed":["39099191"],"doi":["10.1080/10985549.2024.2382453"]}}