http://purl.uniprot.org/citations/19220851 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/19220851 | http://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/19220851 | http://purl.org/dc/terms/identifier | "doi:10.1111/j.1742-4658.2009.06900.x"xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Zhao H."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Nordheim A."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Madlung J."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Lamkemeyer T."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Offermanns S."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Ruth P."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Jakob A."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Korth M."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Sausbier U."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Shipston M.J."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Sausbier M."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Zhou X.B."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Wirth A."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Neuhuber W."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Bucurenciu I."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Pankert P."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/author | "Sprossmann F."xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/name | "FEBS J"xsd:string |
http://purl.uniprot.org/citations/19220851 | http://purl.uniprot.org/core/pages | "1680-1697"xsd:string |
http://purl.uniprot.org/citations/19220851 | http://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/19220851 | http://purl.uniprot.org/core/volume | "276"xsd:string |