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http://purl.uniprot.org/citations/19220851http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19220851http://www.w3.org/2000/01/rdf-schema#comment"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-type Ca(2+) current density and increased expression of cAMP kinase (protein kinase A; PKA), as compared with control mice. Increased expression of PKA in BK(-/-) mice was accompanied by enhanced beta-adrenoceptor/cAMP-mediated suppression of contractions by isoproterenol. This effect was attenuated by about 60-70% in SM-BK(-/-) mice. However, the Rp isomer of adenosine-3',5'-cyclic monophosphorothioate, a blocker of PKA, only partially inhibited enhanced cAMP signaling in BK(-/-) detrusor muscle, suggesting the existence of additional compensatory pathways. To this end, proteome analysis of BK(-/-) urinary bladder tissue was performed, and revealed additional compensatory regulated proteins. Thus, constitutive and inducible deletion of BK channel activity unmasks compensatory mechanisms that are relevant for urinary bladder relaxation."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.org/dc/terms/identifier"doi:10.1111/j.1742-4658.2009.06900.x"xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Zhao H."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Nordheim A."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Madlung J."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Lamkemeyer T."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Offermanns S."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Ruth P."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Jakob A."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Korth M."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Sausbier U."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Shipston M.J."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Sausbier M."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Zhou X.B."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Wirth A."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Neuhuber W."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Bucurenciu I."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Pankert P."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/author"Sprossmann F."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/name"FEBS J"xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/pages"1680-1697"xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/title"Inducible knockout mutagenesis reveals compensatory mechanisms elicited by constitutive BK channel deficiency in overactive murine bladder."xsd:string
http://purl.uniprot.org/citations/19220851http://purl.uniprot.org/core/volume"276"xsd:string