<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pannkuk EL</submitter><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>613-625</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9214627</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>197(6)</volume><pubmed_abstract>Several diagnostic biodosimetry tools have been in development that may aid in radiological/nuclear emergency responses. Of these, correlating changes in non-invasive biofluid small-molecule signatures to tissue damage from ionizing radiation exposure show promise for inclusion in predictive biodosimetry models. Integral to dose reconstruction has been determining how genotypic variation in the general population will affect model performance. Here, we used a mouse model that lacks the T-cell receptor specific alternative p38 pathway [p38αβY323F, double knock-in (DKI) mice] to determine how attenuated autoimmune and inflammatory responses may affect dose reconstruction. We exposed adult male DKI mice (8-10 weeks old) to 2 and 7 Gy in parallel with wild-type mice and assessed perturbations </pubmed_abstract><journal>Radiation research</journal><pubmed_title>Small Molecule Signatures of Mice Lacking T-cell p38 Alternate Activation, a Model for Immunosuppression Conditions, after Total-Body Irradiation.</pubmed_title><pmcid>PMC9214627</pmcid><funding_grant_id>U19 AI067773</funding_grant_id><funding_grant_id>P30 CA051008</funding_grant_id><pubmed_authors>Laiakis EC</pubmed_authors><pubmed_authors>Angdisen J</pubmed_authors><pubmed_authors>Lin LY</pubmed_authors><pubmed_authors>Fornace AJ</pubmed_authors><pubmed_authors>Li HH</pubmed_authors><pubmed_authors>Ake P</pubmed_authors><pubmed_authors>Pannkuk EL</pubmed_authors><pubmed_authors>Jayatilake MM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Small Molecule Signatures of Mice Lacking T-cell p38 Alternate Activation, a Model for Immunosuppression Conditions, after Total-Body Irradiation.</name><description>Several diagnostic biodosimetry tools have been in development that may aid in radiological/nuclear emergency responses. Of these, correlating changes in non-invasive biofluid small-molecule signatures to tissue damage from ionizing radiation exposure show promise for inclusion in predictive biodosimetry models. Integral to dose reconstruction has been determining how genotypic variation in the general population will affect model performance. Here, we used a mouse model that lacks the T-cell receptor specific alternative p38 pathway [p38αβY323F, double knock-in (DKI) mice] to determine how attenuated autoimmune and inflammatory responses may affect dose reconstruction. We exposed adult male DKI mice (8-10 weeks old) to 2 and 7 Gy in parallel with wild-type mice and assessed perturbations </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-21T21:55:51.695Z</modification><creation>2025-04-21T21:55:51.695Z</creation></dates><accession>S-EPMC9214627</accession><cross_references><pubmed>35245386</pubmed><doi>10.1667/rade-21-00199.1</doi><doi>10.1667/RADE-21-00199.1</doi></cross_references></HashMap>