IndraLab

Statements


MINK1 activates KCNH2. 6 / 6
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"Although MinK most likely functions as the accessory subunit for KCNQ1 to form I Ks channels in the heart [XREF_BIBR, XREF_BIBR], MinK can also modulate hERG1 channel density when overexpressed in heterologous expression systems [XREF_BIBR, XREF_BIBR]."

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"MinK increases hERG currents by an unknown mechanism."

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"In addition, D76N and D85N KCNE1 (Mink) mutations also increased the in vitro sensitivity of IKr and hERG to inhibition by clarithromycin [XREF_BIBR]."

"Herg, a human homologue of the ether-a-go-go gene of the fruitfly drosophila melanogaster, encodes aproteinthat produces the rapidly activating cardiac delayed rectifier (i[kr]). / our results show that mink physically associates with herg and that the interaction leads to increased ikr current density."

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"MiRP1 encoded by KCNE2 is thought to regulate KCNH2 in the human heart; MinK encoded by KCNE1 may also modulate KCNH2 in vivo; 14-3-3epsilon binding to KCNH2 channels shifts the activation curve towar[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"These studies indicate that, as in KVLQT1, mutations in minK can cause both autosomal dominant (Romano-Ward syndrome) and autosomal-recessive (JLN) LQT.Identification of SCN5A, HERG, KVLQT1 and minK a[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"