<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee Y</submitter><funding>NINDS NIH HHS</funding><funding>National Institutes of Health</funding><funding>W M Keck Foundation</funding><pagination>411-421</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11624092</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>123</volume><pubmed_abstract>Interleukin-1β (IL1), a pleiotropic cytokine, is involved in sleep regulation, tumor ontogeny, and immune responses. IL1 receptor adaptor proteins, including the IL1 receptor accessory protein (AcP), and its neuron-specific isoform, AcPb, are required for IL1 signaling. The AcPb isoform is resultant from alternate splicing of the AcP transcript. Our previous studies using AcPb null (AcPb&lt;sup>-/-&lt;/sup>) mice characterized its participation in sleep regulation and emergent neuronal/glial network properties. Here, we investigated the impact of acute sleep disruption (SD) on brain cancer-related pathways in wild-type (WT) and AcPb&lt;sup>-/-&lt;/sup> mice, employing RNA sequencing methods. In WT mice, SD increased AcPb mRNA levels, but not AcP mRNA, confirming prior similar work in rats. Transcripto</pubmed_abstract><journal>Brain, behavior, and immunity</journal><pubmed_title>Sleep loss-induced oncogenic pathways are mediated via the neuron-specific interleukin-1 receptor accessory protein (AcPb).</pubmed_title><pmcid>PMC11624092</pmcid><funding_grant_id>R01 NS025378</funding_grant_id><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Schwartzmann CM</pubmed_authors><pubmed_authors>Krueger JM</pubmed_authors><pubmed_authors>English EL</pubmed_authors><pubmed_authors>Lee Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sleep loss-induced oncogenic pathways are mediated via the neuron-specific interleukin-1 receptor accessory protein (AcPb).</name><description>Interleukin-1β (IL1), a pleiotropic cytokine, is involved in sleep regulation, tumor ontogeny, and immune responses. IL1 receptor adaptor proteins, including the IL1 receptor accessory protein (AcP), and its neuron-specific isoform, AcPb, are required for IL1 signaling. The AcPb isoform is resultant from alternate splicing of the AcP transcript. Our previous studies using AcPb null (AcPb&lt;sup>-/-&lt;/sup>) mice characterized its participation in sleep regulation and emergent neuronal/glial network properties. Here, we investigated the impact of acute sleep disruption (SD) on brain cancer-related pathways in wild-type (WT) and AcPb&lt;sup>-/-&lt;/sup> mice, employing RNA sequencing methods. In WT mice, SD increased AcPb mRNA levels, but not AcP mRNA, confirming prior similar work in rats. Transcripto</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan</publication><modification>2026-07-15T13:51:51.334Z</modification><creation>2026-07-05T03:11:30.004Z</creation></dates><accession>S-EPMC11624092</accession><cross_references><pubmed>39343106</pubmed><doi>10.1016/j.bbi.2024.09.029</doi></cross_references></HashMap>