{"doi":"10.1523/jneurosci.17-04-01350.1997","title":"Ligand-Gated Ion Channel Subunit Partnerships: GABA<sub>A</sub>Receptor α<sub>6</sub>Subunit Gene Inactivation Inhibits δ Subunit Expression","abstract":"<jats:p>Cerebellar granule cells express six GABA<jats:sub>A</jats:sub>receptor subunits abundantly (α<jats:sub>1</jats:sub>, α<jats:sub>6</jats:sub>, β<jats:sub>2</jats:sub>, β<jats:sub>3</jats:sub>, γ<jats:sub>2</jats:sub>, and δ) and assemble various pentameric receptor subtypes with unknown subunit compositions; however, the rules guiding receptor subunit assembly are unclear. Here, removal of intact α<jats:sub>6</jats:sub>protein from cerebellar granule cells allowed perturbations in other subunit levels to be studied. Exon 8 of the mouse α<jats:sub>6</jats:sub>subunit gene was disrupted by homologous recombination. In α<jats:sub>6</jats:sub>−/− granule cells, the δ subunit was selectively degraded as seen by immunoprecipitation, immunocytochemistry, and immunoblot analysis with δ subunit-specific antibodies. The δ subunit mRNA was present at wild-type levels in the mutant granule cells, indicating a post-translational loss of the δ subunit. These results provide genetic evidence for a specific association between the α<jats:sub>6</jats:sub>and δ subunits. Because in α<jats:sub>6</jats:sub>−/− neurons the remaining α<jats:sub>1</jats:sub>, β<jats:sub>2/3</jats:sub>, and γ<jats:sub>2</jats:sub>subunits cannot rescue the δ subunit, certain potential subunit combinations may not be found in wild-type cells.</jats:p>","journal":"The Journal of Neuroscience","year":1997,"id":24852,"datarank":11.969383007871773,"base_score":5.771441123130016,"endowment":5.771441123130016,"self_citation_contribution":0.8657161684695025,"citation_network_contribution":11.10366683940227,"self_endowment_contribution":0.8657161684695025,"citer_contribution":11.10366683940227,"corpus_percentile":null,"corpus_rank":null,"citation_count":320,"citer_count":200,"citers_with_citation_signal":200,"citers_with_endowment":200,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":147892,"name":"E. 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Somogyi","orcid":null,"position":12,"is_corresponding":false},{"id":147904,"name":"A. J. H. Smith","orcid":null,"position":13,"is_corresponding":false},{"id":147905,"name":"W. Wisden","orcid":null,"position":14,"is_corresponding":false},{"id":147891,"name":"A. Jones","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":5.771441123130016,"endowment":5.771441123130016,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"9006978","pmcid":"PMC6793744","openalex_id":"https://openalex.org/W1563564990","authors":[],"funders":[],"total_grants":0,"fwci":7.3707,"citation_percentile":0.98406248,"influential_citations":17,"citation_trend":[{"year":2012,"count":8},{"year":2013,"count":7},{"year":2014,"count":9},{"year":2015,"count":4},{"year":2016,"count":7},{"year":2017,"count":7},{"year":2018,"count":5},{"year":2019,"count":5},{"year":2020,"count":3},{"year":2021,"count":2},{"year":2022,"count":1},{"year":2023,"count":8},{"year":2024,"count":2},{"year":2025,"count":1}],"oa_status":"bronze","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","oa_locations":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/6793744","host_type":"repository"},{"url":"https://www.jneurosci.org/content/jneuro/17/4/1350.full.pdf","host_type":"HYBRID"},{"url":"https://www.jneurosci.org/content/jneuro/17/4/1350.full.pdf","host_type":"publisher"},{"url":"https://syndication.highwire.org/content/doi/10.1523/JNEUROSCI.17-04-01350.1997","host_type":"publisher"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9006978","host_type":"repository"}],"fields_of_study":["Neuroscience and Neuropharmacology Research","Ion channel regulation and function","Nicotinic Acetylcholine Receptors Study","Biology","Medicine","Chemistry","Animals","Behavior, Animal","Benzodiazepines","Cerebellum","GABA Agonists","GABA Antagonists","GABA-A Receptor Antagonists","Gene Expression Regulation","Ion Channel Gating","Ion Channels","Lac Operon","Ligands","Male","Mice","Mice, Knockout","Muscimol","Neurons","Protein Processing, Post-Translational","Pyridazines","RNA, Messenger","Receptors, GABA-A"],"mesh_terms":["Animals","Behavior, Animal","Benzodiazepines","Cerebellum","Gene Expression Regulation","Ion Channels","Lac Operon","Ligands","Male","Muscimol","Neurons","Protein Processing, Post-Translational","Pyridazines","Receptors, GABA-A","RNA, Messenger","Ion Channel Gating","Mice, Knockout","GABA Agonists","GABA Antagonists","Mice","GABA-A Receptor Antagonists"],"keywords":["Gamma-aminobutyric acid receptor subunit alpha-1","Protein subunit","Interleukin 10 receptor, alpha subunit","Specificity factor","Interleukin 12 receptor, beta 1 subunit","Interleukin 5 receptor alpha subunit","Biology","Molecular biology","Cell biology","G alpha subunit","Gene","Biochemistry","Gene expression"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Partnerships for the goals"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[{"name":"gen"}],"source":"live","citation_network_status":"fetched"},"created_at":"2026-06-07T23:22:40.273433Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}