{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wong HK"],"funding":["Wellcome Trust"],"pagination":["8732-47"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1265744"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(19)"],"pubmed_abstract":["The c-Jun N-terminal protein kinase (JNK)/c-Jun and p53 pathways form distinct death-signaling modules in neurons that culminate in Bax-dependent apoptosis. To investigate whether this signaling autonomy is due to recruitment of particular BH3-only proteins, we searched for a toxic signal that would activate both pathways in the same set of neurons. We show that arsenite activates both the JNK/c-Jun and p53 pathways in cortical neurons, which together account for >95% of apoptosis, as determined by using the mixed-lineage kinase (JNK/c-Jun) pathway inhibitor CEP11004 and p53-null mice. Despite the coexistence of both pathways in at least 30% of the population, Bim mRNA and protein expression was increased only by the JNK/c-Jun signaling pathway, whereas Noxa and Puma mRNA and Puma protein "],"journal":["Molecular and cellular biology"],"pubmed_title":["Mutually exclusive subsets of BH3-only proteins are activated by the p53 and c-Jun N-terminal kinase/c-Jun signaling pathways during cortical neuron apoptosis induced by arsenite."],"pmcid":["PMC1265744"],"funding_grant_id":["064232"],"pubmed_authors":["Fricker M","Villunger A","Wyttenbach A","Wong HK","Michalak EM","Tolkovsky AM","Strasser A"],"additional_accession":[]},"is_claimable":false,"name":"Mutually exclusive subsets of BH3-only proteins are activated by the p53 and c-Jun N-terminal kinase/c-Jun signaling pathways during cortical neuron apoptosis induced by arsenite.","description":"The c-Jun N-terminal protein kinase (JNK)/c-Jun and p53 pathways form distinct death-signaling modules in neurons that culminate in Bax-dependent apoptosis. To investigate whether this signaling autonomy is due to recruitment of particular BH3-only proteins, we searched for a toxic signal that would activate both pathways in the same set of neurons. We show that arsenite activates both the JNK/c-Jun and p53 pathways in cortical neurons, which together account for >95% of apoptosis, as determined by using the mixed-lineage kinase (JNK/c-Jun) pathway inhibitor CEP11004 and p53-null mice. Despite the coexistence of both pathways in at least 30% of the population, Bim mRNA and protein expression was increased only by the JNK/c-Jun signaling pathway, whereas Noxa and Puma mRNA and Puma protein ","dates":{"release":"2005-01-01T00:00:00Z","publication":"2005 Oct","modification":"2025-04-25T21:30:14.014Z","creation":"2019-06-06T22:24:58Z"},"accession":"S-EPMC1265744","cross_references":{"pubmed":["16166651"],"doi":["10.1128/mcb.25.19.8732-8747.2005","10.1128/MCB.25.19.8732-8747.2005"]}}