Ankyrin B Modulates the Function of Na,K-ATPase/Inositol 1,4,5-Trisphosphate Receptor Signaling MicrodomainVisa övriga samt affilieringar
2008 (Engelska)Ingår i: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 283, nr 17, s. 11461-11468Artikel i tidskrift (Refereegranskat) Published
Abstract [en]
Na, K-ATPase and inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) can form a signaling microdomain that in the presence of ouabain triggers highly regular calcium oscillations. Downstream effects include NF-kappa B activation. Here we report that ankyrin B (Ank-B), expressed in most mammalian cells, plays a pivotal role in the function of the Na, K-ATPase/ IP3R signaling microdomain. In studies performed on a monkey kidney cell line, we show that Ank-B co-precipitates with both Na, K-ATPase and IP3R. We identify the N terminus tail of the Na, K-ATPase catalytic subunit and the N-terminal portion 1-604 of the IP3R as novel binding sites for Ank-B. Knockdown of Ank-B with small interfering RNA reduced the expression of Ank-B to 15-30%. This down-regulation of Ank-B attenuated the interaction between Na, K-ATPase and IP3R, reduced the number of cells responding to pM doses of ouabain with calcium oscillations, altered the calcium oscillatory pattern, and abolished the ouabain effect on NF-kappa B. In contrast, Ank-B down-regulation had no effect on the ion transporting function of Na, K-ATPase and no effect on the distribution and apparent mobility of Na, K-ATPase in the plasma membrane.
Ort, förlag, år, upplaga, sidor
2008. Vol. 283, nr 17, s. 11461-11468
Nyckelord [en]
generates calcium oscillations, nf-kappa-b, cardiac-arrhythmia, catalytic subunit, serum deprivation, binding domain, na+/k+-atpase, ip3 receptor, na, k-atpase, identification
Nationell ämneskategori
Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)
Identifikatorer
URN: urn:nbn:se:kth:diva-11817DOI: 10.1074/jbc.M706942200ISI: 000255067400044PubMedID: 18303017Scopus ID: 2-s2.0-45549103740OAI: oai:DiVA.org:kth-11817DiVA, id: diva2:283474
Anmärkning
QC 20100806
2009-12-282009-12-282022-06-25Bibliografiskt granskad
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