<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shim J</submitter><funding>Institutional Developmental Award from the National Institute of General Medical Sciences of the National Institutes of Health</funding><funding>USDA National Institute of Food and Agriculture, Maine Agricultural and Forest Experiment Station</funding><funding>NIGMS NIH HHS</funding><pagination>1446-59</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5040607</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(11)</volume><pubmed_abstract>Exposure to arsenic is a global health concern. We previously documented an inhibitory effect of inorganic Arsenite on IgE-mediated degranulation of RBL-2H3 mast cells (Hutchinson et al., 2011; J. Appl. Toxicol. 31: 231-241). Mast cells are tissue-resident cells that are positioned at the host-environment interface, thereby serving vital roles in many physiological processes and disease states, in addition to their well-known roles in allergy and asthma. Upon activation, mast cells secrete several mediators from cytoplasmic granules, in degranulation. The present study is an investigation of Arsenite's molecular target(s) in the degranulation pathway. Here, we report that arsenic does not affect degranulation stimulated by either the Ca(2) (+) ionophore A23187 or thapsigargin, which both b</pubmed_abstract><journal>Journal of applied toxicology : JAT</journal><pubmed_title>Arsenic inhibits mast cell degranulation via suppression of early tyrosine phosphorylation events.</pubmed_title><pmcid>PMC5040607</pmcid><funding_grant_id>P20 GM103423</funding_grant_id><funding_grant_id>ME08004-10</funding_grant_id><funding_grant_id>P20-GM103423</funding_grant_id><pubmed_authors>Velez A</pubmed_authors><pubmed_authors>Weatherly LM</pubmed_authors><pubmed_authors>Kennedy RH</pubmed_authors><pubmed_authors>Blais K</pubmed_authors><pubmed_authors>Hutchinson LM</pubmed_authors><pubmed_authors>Hashmi HN</pubmed_authors><pubmed_authors>Gosse JA</pubmed_authors><pubmed_authors>Shim J</pubmed_authors><pubmed_authors>Pelletier JH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Arsenic inhibits mast cell degranulation via suppression of early tyrosine phosphorylation events.</name><description>Exposure to arsenic is a global health concern. We previously documented an inhibitory effect of inorganic Arsenite on IgE-mediated degranulation of RBL-2H3 mast cells (Hutchinson et al., 2011; J. Appl. Toxicol. 31: 231-241). Mast cells are tissue-resident cells that are positioned at the host-environment interface, thereby serving vital roles in many physiological processes and disease states, in addition to their well-known roles in allergy and asthma. Upon activation, mast cells secrete several mediators from cytoplasmic granules, in degranulation. The present study is an investigation of Arsenite's molecular target(s) in the degranulation pathway. Here, we report that arsenic does not affect degranulation stimulated by either the Ca(2) (+) ionophore A23187 or thapsigargin, which both b</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Nov</publication><modification>2025-04-04T00:21:24.972Z</modification><creation>2019-03-27T02:25:24Z</creation></dates><accession>S-EPMC5040607</accession><cross_references><pubmed>27018130</pubmed><doi>10.1002/jat.3300</doi></cross_references></HashMap>