IndraLab

Statements

SIGMAR1 activates KCNH2. 10 / 10
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"Heterologous expression in Xenopus oocytes demonstrates that Sig1R potentiates hERG current by stimulating channel subunit biosynthesis."
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"Sigma 1 R potentiates hERG current by stimulating channel subunit biosynthesis and sigma 1 R silencing does not modify hERG mRNA contents but reduces hERG mature form densities."
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"Sigma-1R was shown to promote humanEther-a-go-go-RelatedGene (hERG) protein expression within the plasma membrane."
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"Delving into the molecular mechanisms, we observed that the silencing of Sig1R decreases hERG maturation efficiency and diminishes the alpha-subunit channel stability at the plasma membrane, in turn reducing the number of ion channels available."
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"However, while Balasuriya et al., 2014 XREF_BIBR proposed that Sigma-1R binds to an immature hERG in the ER and reduces expression of mature hERG, Johannessen et al, 2009, suggested that sigma-1R expression enhances hERG protein maturation and stability, by regulating subunit trafficking activity of hERG XREF_BIBR."
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"In human leukaemic cells, our group found that the silencing of Sig1R by shRNA reduces the endogenous human ether-a-gogo-related gene (hERG; Kv11.1) current density without altering channel voltage dependency or kinetic parameters."
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"As stated above, we recently showed that Sig1R expression stimulates hERG maturation and membrane stability in the chronic myeloid leukaemia cell line K562."
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"Sigmar1 increased hERG current density via a regulation of channel subunit maturation and stability in a chronic myeloid cell line (K562), HEK-293 cells, and Xenopus oocytes (Crottes et al., 2011)."
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"In addition, SIGMAR1 silencing using shRNA or the treatment of progesterone, which is also known as a SIGMAR1 antagonist, decreased hERG current density and negatively regulated the membrane expression of hERG channel in leukemic cells, HEK cells and neonatal rat cardiomyocytes while SIGMAR1 overexpression potentiated hERG current density in Xenopus oocytes ."
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"Sig1R promoted the formation of hERG and beta1-integrin signaling complexes upon extracellular matrix stimulation, triggering the activation of the PI3K and AKT pathway."
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