<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>61(2)</volume><submitter>Gomi H</submitter><pubmed_abstract>Islet-associated protein-2 (IA-2) and IA-2? (also known as phogrin) are unique neuroendocrine-specific protein tyrosine phosphatases (PTPs). The IA-2 family of PTPs was originally identified from insulinoma cells and discovered to be major autoantigens in type 1 diabetes. Despite its expression in the neural and canonical endocrine tissues, data on expression of the IA-2 family of PTPs in gastrointestinal endocrine cells (GECs) are limited. Therefore, we immunohistochemically investigated the expression of the IA-2 family of PTPs in the rat gastrointestinal tract. In the stomach, IA-2 and IA-2? were expressed in GECs that secrete serotonin, somatostatin, and cholecystokinin/gastrin-1. In addition to these hormones, secretin, gastric inhibitory polypeptide (also known as the glucose-dependent insulinotropic peptide), glucagon-like peptide-1, and glucagon, but not ghrelin were coexpressed with IA-2 or IA-2? in duodenal GECs. Pancreatic islet cells that secrete gut hormones expressed the IA-2 family of PTPs. The expression patterns of IA-2 and IA-2? were comparable. These results reveal that the IA-2 family of PTPs is expressed in a cell type-specific manner in rat GECs. The extensive expression of the IA-2 family of PTPs in pancreo-gastrointestinal endocrine cells and in the enteric plexus suggests their systemic contribution to nutritional control through a neuroendocrine signaling network.</pubmed_abstract><journal>The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society</journal><pagination>156-68</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3636693</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Immunohistochemical analysis of IA-2 family of protein tyrosine phosphatases in rat gastrointestinal endocrine cells.</pubmed_title><pmcid>PMC3636693</pmcid><pubmed_authors>Torii S</pubmed_authors><pubmed_authors>Yasui T</pubmed_authors><pubmed_authors>Kubota-Murata C</pubmed_authors><pubmed_authors>Gomi H</pubmed_authors><pubmed_authors>Tsukise A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immunohistochemical analysis of IA-2 family of protein tyrosine phosphatases in rat gastrointestinal endocrine cells.</name><description>Islet-associated protein-2 (IA-2) and IA-2? (also known as phogrin) are unique neuroendocrine-specific protein tyrosine phosphatases (PTPs). The IA-2 family of PTPs was originally identified from insulinoma cells and discovered to be major autoantigens in type 1 diabetes. Despite its expression in the neural and canonical endocrine tissues, data on expression of the IA-2 family of PTPs in gastrointestinal endocrine cells (GECs) are limited. Therefore, we immunohistochemically investigated the expression of the IA-2 family of PTPs in the rat gastrointestinal tract. In the stomach, IA-2 and IA-2? were expressed in GECs that secrete serotonin, somatostatin, and cholecystokinin/gastrin-1. In addition to these hormones, secretin, gastric inhibitory polypeptide (also known as the glucose-dependent insulinotropic peptide), glucagon-like peptide-1, and glucagon, but not ghrelin were coexpressed with IA-2 or IA-2? in duodenal GECs. Pancreatic islet cells that secrete gut hormones expressed the IA-2 family of PTPs. The expression patterns of IA-2 and IA-2? were comparable. These results reveal that the IA-2 family of PTPs is expressed in a cell type-specific manner in rat GECs. The extensive expression of the IA-2 family of PTPs in pancreo-gastrointestinal endocrine cells and in the enteric plexus suggests their systemic contribution to nutritional control through a neuroendocrine signaling network.</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Feb</publication><modification>2021-03-06T08:29:40Z</modification><creation>2019-03-27T01:07:56Z</creation></dates><accession>S-EPMC3636693</accession><cross_references><pubmed>23087044</pubmed><doi>10.1369/0022155412466872</doi></cross_references></HashMap>