{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sprossmann F"],"funding":["Wellcome Trust"],"pagination":["1680-97"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4025950"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["276(6)"],"pubmed_abstract":["The large-conductance, voltage-dependent and Ca(2+)-dependent K(+) (BK) channel links membrane depolarization and local increases in cytosolic free Ca(2+) to hyperpolarizing K(+) outward currents, thereby controlling smooth muscle contractility. Constitutive deletion of the BK channel in mice (BK(-/-)) leads to an overactive bladder associated with increased intravesical pressure and frequent micturition, which has been revealed to be a result of detrusor muscle hyperexcitability. Interestingly, time-dependent and smooth muscle-specific deletion of the BK channel (SM-BK(-/-)) caused a more severe phenotype than displayed by constitutive BK(-/-) mice, suggesting that compensatory pathways are active in the latter. In detrusor muscle of BK(-/-) but not SM-BK(-/-) mice, we found reduced L-typ"],"journal":["The FEBS journal"],"pubmed_title":["Inducible knockout mutagenesis reveals compensatory mechanisms elicited by constitutive BK channel deficiency in overactive murine bladder."],"pmcid":["PMC4025950"],"funding_grant_id":["082407"],"pubmed_authors":["Jakob A","Lamkemeyer T","Sausbier M","Zhou XB","Nordheim A","Sprossmann F","Wirth A","Sausbier U","Ruth P","Pankert P","Korth M","Bucurenciu I","Neuhuber W","Madlung J","Zhao H","Offermanns S","Shipston MJ"],"additional_accession":[]},"is_claimable":false,"name":"Inducible knockout mutagenesis reveals compensatory mechanisms elicited by constitutive BK channel deficiency in overactive murine bladder.","description":"The large-conductance, voltage-dependent and Ca(2+)-dependent K(+) (BK) channel links membrane depolarization and local increases in cytosolic free Ca(2+) to hyperpolarizing K(+) outward currents, thereby controlling smooth muscle contractility. Constitutive deletion of the BK channel in mice (BK(-/-)) leads to an overactive bladder associated with increased intravesical pressure and frequent micturition, which has been revealed to be a result of detrusor muscle hyperexcitability. Interestingly, time-dependent and smooth muscle-specific deletion of the BK channel (SM-BK(-/-)) caused a more severe phenotype than displayed by constitutive BK(-/-) mice, suggesting that compensatory pathways are active in the latter. In detrusor muscle of BK(-/-) but not SM-BK(-/-) mice, we found reduced L-typ","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Mar","modification":"2025-04-04T08:42:11.401Z","creation":"2019-03-27T01:28:30Z"},"accession":"S-EPMC4025950","cross_references":{"pubmed":["19220851"],"doi":["10.1111/j.1742-4658.2009.06900.x"]}}