{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hart M"],"funding":["Deutsche Forschungsgemeinschaft","EC | Seventh Framework Programme","Michael J. Fox Foundation for Parkinson's Research"],"pagination":["46"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6362007"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(2)"],"pubmed_abstract":["NF-κB functions as modulator of T cell receptor-mediated signaling and transcriptional regulator of miR-34a. Our in silico analysis revealed that miR-34a impacts the NF-κB signalosome with miR-34a binding sites in 14 key members of the NF-κB signaling pathway. Functional analysis identified five target genes of miR-34a including PLCG1, CD3E, PIK3CB, TAB2, and NFΚBIA. Overexpression of miR-34a in CD4+ and CD8+ T cells led to a significant decrease of NFΚBIA as the most downstream cytoplasmic NF-κB member, a reduced cell surface abundance of TCRA and CD3E, and to a reduction of T cell killing capacity. Inhibition of miR-34a caused an increase of NFΚBIA, TCRA, and CD3E. Notably, activation of CD4+ and CD8+ T cells entrails a gradual increase of miR-34a. Our results lend further support to a model with miR-34a as a central NF-κB regulator in T cells."],"journal":["Cell death & disease"],"pubmed_title":["miR-34a: a new player in the regulation of T cell function by modulation of NF-κB signaling."],"pmcid":["PMC6362007"],"funding_grant_id":["SFB894"],"pubmed_authors":["Hart M","Walch-Ruckheim B","Tanzer T","Keller A","Glombitza B","Friedmann KS","Rheinheimer S","Lenhof HP","Hoth M","Meese E","Sester M","Schwarz EC"],"additional_accession":[]},"is_claimable":false,"name":"miR-34a: a new player in the regulation of T cell function by modulation of NF-κB signaling.","description":"NF-κB functions as modulator of T cell receptor-mediated signaling and transcriptional regulator of miR-34a. Our in silico analysis revealed that miR-34a impacts the NF-κB signalosome with miR-34a binding sites in 14 key members of the NF-κB signaling pathway. Functional analysis identified five target genes of miR-34a including PLCG1, CD3E, PIK3CB, TAB2, and NFΚBIA. Overexpression of miR-34a in CD4+ and CD8+ T cells led to a significant decrease of NFΚBIA as the most downstream cytoplasmic NF-κB member, a reduced cell surface abundance of TCRA and CD3E, and to a reduction of T cell killing capacity. Inhibition of miR-34a caused an increase of NFΚBIA, TCRA, and CD3E. Notably, activation of CD4+ and CD8+ T cells entrails a gradual increase of miR-34a. Our results lend further support to a model with miR-34a as a central NF-κB regulator in T cells.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jan","modification":"2025-04-25T17:25:44.971Z","creation":"2019-03-26T22:50:47Z"},"accession":"S-EPMC6362007","cross_references":{"pubmed":["30718475"],"doi":["10.1038/s41419-018-1295-1"]}}