{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sun H"],"funding":["NIMH NIH HHS"],"pagination":["4934"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4017216"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4"],"pubmed_abstract":["Current technologies for studying ion channels are fundamentally limited because of their inability to functionally link ion channel activity to cellular pathways. Herein, we report the use of label-free cell phenotypic profiling to decode the composition and signaling of an endogenous ATP-sensitive potassium ion channel (KATP) in HepG2C3A, a hepatocellular carcinoma cell line. Label-free cell phenotypic agonist profiling showed that pinacidil triggered characteristically similar dynamic mass redistribution (DMR) signals in A431, A549, HT29 and HepG2C3A, but not in HepG2 cells. Reverse transcriptase PCR, RNAi knockdown, and KATP blocker profiling showed that the pinacidil DMR is due to the activation of SUR2/Kir6.2 KATP channels in HepG2C3A cells. Kinase inhibition and RNAi knockdown showe"],"journal":["Scientific reports"],"pubmed_title":["Label-free cell phenotypic profiling decodes the composition and signaling of an endogenous ATP-sensitive potassium channel."],"pmcid":["PMC4017216"],"funding_grant_id":["U54 MH084691","5U54MH084691"],"pubmed_authors":["Fang Y","Xiong Q","Sun H","Wei Y","Lahiri J","Deng H","Li M"],"additional_accession":[]},"is_claimable":false,"name":"Label-free cell phenotypic profiling decodes the composition and signaling of an endogenous ATP-sensitive potassium channel.","description":"Current technologies for studying ion channels are fundamentally limited because of their inability to functionally link ion channel activity to cellular pathways. Herein, we report the use of label-free cell phenotypic profiling to decode the composition and signaling of an endogenous ATP-sensitive potassium ion channel (KATP) in HepG2C3A, a hepatocellular carcinoma cell line. Label-free cell phenotypic agonist profiling showed that pinacidil triggered characteristically similar dynamic mass redistribution (DMR) signals in A431, A549, HT29 and HepG2C3A, but not in HepG2 cells. Reverse transcriptase PCR, RNAi knockdown, and KATP blocker profiling showed that the pinacidil DMR is due to the activation of SUR2/Kir6.2 KATP channels in HepG2C3A cells. Kinase inhibition and RNAi knockdown showe","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 May","modification":"2026-05-02T00:11:30.941Z","creation":"2019-03-27T01:27:58Z"},"accession":"S-EPMC4017216","cross_references":{"pubmed":["24816792"],"doi":["10.1038/srep04934"]}}