<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(1)</volume><submitter>Zhang W</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Atrial natriuretic peptide (ANP) is an important endogenous hormone that controls inflammation and immunity by acting on dendritic cells (DCs); however, the mechanism remains unclear.&lt;h4>Objective&lt;/h4>We analyzed the downstream signaling events resulting from the binding of ANP to its receptor, NPRA, and sought to determine what aspects of this signaling modulate DC function.&lt;h4>Methods&lt;/h4>We utilized the inhibitory peptide, NP73-102, to block NPRA signaling in human monocyte-derived DCs (hmDCs) and examined the effect on DC maturation and induced immune responses. The potential downstream molecules and interactions among these molecules involved in NPRA signaling were identified by immunoprecipitation and immunoblotting. Changes in T cell phenotype and function were de</pubmed_abstract><journal>Genetic vaccines and therapy</journal><pagination>3</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3025824</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Plasmid-encoded NP73-102 modulates atrial natriuretic peptide receptor signaling and plays a critical role in inducing tolerogenic dendritic cells.</pubmed_title><pmcid>PMC3025824</pmcid><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Yang H</pubmed_authors><pubmed_authors>Mohapatra S</pubmed_authors><pubmed_authors>Cao X</pubmed_authors><pubmed_authors>Hellermann G</pubmed_authors><pubmed_authors>Mohapatra SS</pubmed_authors><pubmed_authors>Wang W</pubmed_authors><pubmed_authors>Wang JW</pubmed_authors><pubmed_authors>Lockey RF</pubmed_authors><pubmed_authors>Kong X</pubmed_authors><pubmed_authors>Chen D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Plasmid-encoded NP73-102 modulates atrial natriuretic peptide receptor signaling and plays a critical role in inducing tolerogenic dendritic cells.</name><description>&lt;h4>Background&lt;/h4>Atrial natriuretic peptide (ANP) is an important endogenous hormone that controls inflammation and immunity by acting on dendritic cells (DCs); however, the mechanism remains unclear.&lt;h4>Objective&lt;/h4>We analyzed the downstream signaling events resulting from the binding of ANP to its receptor, NPRA, and sought to determine what aspects of this signaling modulate DC function.&lt;h4>Methods&lt;/h4>We utilized the inhibitory peptide, NP73-102, to block NPRA signaling in human monocyte-derived DCs (hmDCs) and examined the effect on DC maturation and induced immune responses. The potential downstream molecules and interactions among these molecules involved in NPRA signaling were identified by immunoprecipitation and immunoblotting. Changes in T cell phenotype and function were de</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jan</publication><modification>2025-04-19T23:56:23.754Z</modification><creation>2019-03-27T00:38:22Z</creation></dates><accession>S-EPMC3025824</accession><cross_references><pubmed>21219617</pubmed><doi>10.1186/1479-0556-9-3</doi></cross_references></HashMap>