<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Torres E</submitter><funding>NICHD NIH HHS</funding><funding>MEC | Instituto de Salud Carlos III</funding><funding>Ministerio de Economía y Competitividad</funding><funding>EC | Horizon 2020</funding><pagination>E496-E511</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8828271</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>320(3)</volume><pubmed_abstract>Tachykinin (TAC) signaling is an important element in the central control of reproduction. TAC family is mainly composed of substance P (SP), neurokinin A (NKA), and NKB, which bind preferentially to NK1, NK2, and NK3 receptors, respectively. While most studies have focused on the reproductive functions of NKB/NK3R, and to a lesser extent SP/NK1R, the relevance of NK2R, encoded by &lt;i>Tacr2&lt;/i>, remains poorly characterized. Here, we address the physiological roles of NK2R in regulating the reproductive axis by characterizing a novel mouse line with congenital ablation of &lt;i>Tacr2&lt;/i>. Activation of NK2R evoked acute luteinizing hormone (LH) responses in control mice, similar to those of agonists of NK1R and NK3R. Despite the absence of NK2R, &lt;i>Tacr2&lt;/i>&lt;sup>-/-&lt;/sup> mice displayed only p</pubmed_abstract><journal>American journal of physiology. Endocrinology and metabolism</journal><pubmed_title>Congenital ablation of &lt;i>Tacr2&lt;/i> reveals overlapping and redundant roles of NK2R signaling in the control of reproductive axis.</pubmed_title><pmcid>PMC8828271</pmcid><funding_grant_id>R01 HD099084</funding_grant_id><funding_grant_id>REP-655232</funding_grant_id><funding_grant_id>BFU2017-83934-P</funding_grant_id><funding_grant_id>R01 HD090151</funding_grant_id><funding_grant_id>PIE-00005</funding_grant_id><pubmed_authors>Pineda R</pubmed_authors><pubmed_authors>Navarro VM</pubmed_authors><pubmed_authors>Gaytan F</pubmed_authors><pubmed_authors>Candenas ML</pubmed_authors><pubmed_authors>Heras V</pubmed_authors><pubmed_authors>Leon S</pubmed_authors><pubmed_authors>Franssen D</pubmed_authors><pubmed_authors>Tena-Sempere M</pubmed_authors><pubmed_authors>Torres E</pubmed_authors><pubmed_authors>Velasco I</pubmed_authors><pubmed_authors>Romero-Ruiz A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Congenital ablation of &lt;i>Tacr2&lt;/i> reveals overlapping and redundant roles of NK2R signaling in the control of reproductive axis.</name><description>Tachykinin (TAC) signaling is an important element in the central control of reproduction. TAC family is mainly composed of substance P (SP), neurokinin A (NKA), and NKB, which bind preferentially to NK1, NK2, and NK3 receptors, respectively. While most studies have focused on the reproductive functions of NKB/NK3R, and to a lesser extent SP/NK1R, the relevance of NK2R, encoded by &lt;i>Tacr2&lt;/i>, remains poorly characterized. Here, we address the physiological roles of NK2R in regulating the reproductive axis by characterizing a novel mouse line with congenital ablation of &lt;i>Tacr2&lt;/i>. Activation of NK2R evoked acute luteinizing hormone (LH) responses in control mice, similar to those of agonists of NK1R and NK3R. Despite the absence of NK2R, &lt;i>Tacr2&lt;/i>&lt;sup>-/-&lt;/sup> mice displayed only p</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-18T12:11:01.502Z</modification><creation>2025-04-06T21:49:40.75Z</creation></dates><accession>S-EPMC8828271</accession><cross_references><pubmed>33427049</pubmed><doi>10.1152/ajpendo.00346.2020</doi></cross_references></HashMap>