Trafficking of the IKs -Complex in MDCK Cells: Site of Subunit Assembly and Determinants of Polarized Localization
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Trafficking of the IKs -Complex in MDCK Cells : Site of Subunit Assembly and Determinants of Polarized Localization. / David, Jens-Peter; Andersen, Martin N; Olesen, Søren-Peter; Rasmussen, Hanne B; Schmitt, Nicole.
In: Traffic, Vol. 14, No. 4, 04.2013, p. 399-411.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Trafficking of the IKs -Complex in MDCK Cells
T2 - Site of Subunit Assembly and Determinants of Polarized Localization
AU - David, Jens-Peter
AU - Andersen, Martin N
AU - Olesen, Søren-Peter
AU - Rasmussen, Hanne B
AU - Schmitt, Nicole
N1 - © 2013 John Wiley & Sons A/S.
PY - 2013/4
Y1 - 2013/4
N2 - The voltage-gated potassium channel K 7.1 is regulated by non-pore forming regulatory KCNE ß-subunits. Together with KCNE1, it forms the slowly activating delayed rectifier potassium current I . However, where the subunits assemble and which of the subunits determines localization of the I -complex has not been unequivocally resolved yet. We employed trafficking-deficient K 7.1 and KCNE1 mutants to investigate I trafficking using the polarized Madin-Darby Canine Kidney cell line. We find that the assembly happens early in the secretory pathway but provide three lines of evidence that it takes place in a post-endoplasmic reticulum compartment. We demonstrate that K 7.1 targets the I -complex to the basolateral membrane, but that KCNE1 can redirect the complex to the apical membrane upon mutation of critical K 7.1 basolateral targeting signals. Our data provide a possible explanation to the fact that K 7.1 can be localized apically or basolaterally in different epithelial tissues and offer a solution to divergent literature results regarding the effect of KCNE subunits on the subcellular localization of K 7.1/KCNE complexes.
AB - The voltage-gated potassium channel K 7.1 is regulated by non-pore forming regulatory KCNE ß-subunits. Together with KCNE1, it forms the slowly activating delayed rectifier potassium current I . However, where the subunits assemble and which of the subunits determines localization of the I -complex has not been unequivocally resolved yet. We employed trafficking-deficient K 7.1 and KCNE1 mutants to investigate I trafficking using the polarized Madin-Darby Canine Kidney cell line. We find that the assembly happens early in the secretory pathway but provide three lines of evidence that it takes place in a post-endoplasmic reticulum compartment. We demonstrate that K 7.1 targets the I -complex to the basolateral membrane, but that KCNE1 can redirect the complex to the apical membrane upon mutation of critical K 7.1 basolateral targeting signals. Our data provide a possible explanation to the fact that K 7.1 can be localized apically or basolaterally in different epithelial tissues and offer a solution to divergent literature results regarding the effect of KCNE subunits on the subcellular localization of K 7.1/KCNE complexes.
U2 - 10.1111/tra.12042
DO - 10.1111/tra.12042
M3 - Journal article
C2 - 23324056
VL - 14
SP - 399
EP - 411
JO - Traffic
JF - Traffic
SN - 1398-9219
IS - 4
ER -
ID: 45080493