IndraLab

Statements


| 4 2

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"Noteworthy, treating HCT116 cells with E4031 did not affect the formation of the hERG1/PI3K complex (Fig. 3c)."

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"Clarithromycin (CLA), a specific inhibitor of hERG1, preferentially binds to the closed conformation of this ion channel to inhibit hERG1-PI3K complex formation, and therefore reduces Akt phosphorylation, leading to increased autophagic flux."
| PMC

sparser
"Clarithromycin (CLA), a specific inhibitor of hERG1, preferentially binds to the closed conformation of this ion channel to inhibit hERG1-PI3K complex formation, and therefore reduces Akt phosphorylation, leading to increased autophagic flux."
| PMC

sparser
"HERG1 interacts with PI3K, which through PDK1, activates Akt1."
| PMC

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"The beta 1 / hERG1 and PI3K complex, through Akt, induces HIF (s) transcriptional activation."

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"This conclusion is supported by the following observations: (i) the binding of Cla is independent on hERG1 conduction (see the effects on the G628S mutant) and is favored when hERG1 is in a closed conformation (see the effects on the R531C mutant) (Fig. 3e, f); (ii) E4031 alone, which targets the open channel has different effects compared to Cla and to hERG1 knockdown, since it does not affect either the hERG1/PI3K complex (Fig. 3c) or Akt phosphorylation (Fig. 3d)."