{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Acosta-Martinez M"],"funding":["NICHD NIH HHS","NIDDK NIH HHS","PHS HHS"],"pagination":["4203-12"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2736084"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["150(9)"],"pubmed_abstract":["GnRH neurosecretion is subject to regulation by insulin, IGF-I, leptin, and other neuroendocrine modulators whose effects may be conveyed by activation of phosphoinositide 3-kinase (PI3K)-mediated pathways. It is not known, however, whether any of these regulatory actions are exerted directly, via activation of PI3K in GnRH neurons, or whether they are primarily conveyed via effects on afferent circuitries governing GnRH neurosecretion. To investigate the role of PI3K signaling in GnRH neurons, we used conditional gene targeting to ablate expression of the major PI3K regulatory subunit, p85alpha, in GnRH neurons. Combined in situ hybridization and immunohistochemistry confirmed reduction of p85alpha mRNA expression in GnRH neurons of GnRH-p85alpha knockout (KO) animals. Females of both gen"],"journal":["Endocrinology"],"pubmed_title":["Male-biased effects of gonadotropin-releasing hormone neuron-specific deletion of the phosphoinositide 3-kinase regulatory subunit p85alpha on the reproductive axis."],"pmcid":["PMC2736084"],"funding_grant_id":["R01 HD020677","P50 HD044405","P50HD44405","K99 HDO55446","P60 DK079637","R01 HD20677","K99 HD055446"],"pubmed_authors":["Luo J","Levine JE","Elias C","Wolfe A","Acosta-Martinez M"],"additional_accession":[]},"is_claimable":false,"name":"Male-biased effects of gonadotropin-releasing hormone neuron-specific deletion of the phosphoinositide 3-kinase regulatory subunit p85alpha on the reproductive axis.","description":"GnRH neurosecretion is subject to regulation by insulin, IGF-I, leptin, and other neuroendocrine modulators whose effects may be conveyed by activation of phosphoinositide 3-kinase (PI3K)-mediated pathways. It is not known, however, whether any of these regulatory actions are exerted directly, via activation of PI3K in GnRH neurons, or whether they are primarily conveyed via effects on afferent circuitries governing GnRH neurosecretion. To investigate the role of PI3K signaling in GnRH neurons, we used conditional gene targeting to ablate expression of the major PI3K regulatory subunit, p85alpha, in GnRH neurons. Combined in situ hybridization and immunohistochemistry confirmed reduction of p85alpha mRNA expression in GnRH neurons of GnRH-p85alpha knockout (KO) animals. Females of both gen","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Sep","modification":"2025-04-19T05:38:48.717Z","creation":"2019-03-26T23:59:14Z"},"accession":"S-EPMC2736084","cross_references":{"pubmed":["19541766"],"doi":["10.1210/en.2008-1753"]}}