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phosphosite cbn pc11 biopax bel_lc signor biogrid lincs_drug tas hprd trrust ctd virhostnet phosphoelm drugbank omnipath | geneways tees isi trips rlimsp medscan sparser eidos reach
reading

KCNH5 affects MB
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KCNH5 activates MB.
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KCNH5 activates MB. 10 / 10
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"We find that EAG2 channel is enriched at the trailing edge of migrating MB cells to regulate local cell volume dynamics thereby facilitating cell motility, and EAG2 knockdown impairs MB metastasis in a xenograft model."
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"EAG2 upregulation in metastatic MB of subsets of patients."
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"Moreover, EAG2 knockdown markedly reduced the motility of MB cells without affecting directionality, as did the EAG2 channel blocker astemizole, a known EAG2 channel blocker with an IC 50 of ~ 1.5 muM 32 (XREF_FIG)."
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"We demonstrate that pharmacological inhibition of EAG2 reduces MB cell viability and motility, and identify an FDA approved antipsychotic drug, thioridazine, as a novel EAG2 channel blocker with potent efficacy in reducing intracranial xenograft MB growth and metastasis."
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"We identify the FDA approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient."
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"The finding of elevated EAG2 expression in metastatic lesions raised the prospect that EAG2 may promote MB metastasis or tumor growth at the disseminated site."
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"These results demonstrate that EAG2 promotes MB metastasis, a function distinct from its role in driving primary tumor growth."
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"EAG2 knockdown not only impairs MB cell growth in vitro, but also reduces tumor burden in vivo and enhances survival in xenograft studies."
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"In this cancer, EAG-2 promotes the progression of the MB tumor by regulating cell volume dynamics, in turn inhibiting the tumor suppressor p38 MAPK pathway."
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"We identified the FDA approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient."
KCNH5 inhibits MB.
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KCNH5 inhibits MB. 2 / 2
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"The ability of two structurally unrelated EAG2 channel blockers to reduce MB growth in vivo in mouse models, taken together with the specific effects of thioridazine in curbing the growth and metastasis of xenograft human MB with high but not low EAG2 expression, point to EAG2 as a promising target for treatment of MB that displays high EAG2 expression."
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"We provide evidence that the known EAG2 channel blocker astemizole reduces MB cell migratory polarization and cell rear contraction, and impairs MB cell viability, motility and allografted tumor growth (XREF_FIG and XREF_SUPPLEMENTARY)."
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"We identify the FDA approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient."
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"Using multiple Drosophila brain tumor models induced by oncogene overexpression or loss of tumor suppressors to complement our study of mice with xenografted human MB cells, we show that the functions of EAG2 and Eag channel to promote malignant growth and metastasis are evolutionarily conserved (XREF_FIG)."
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"These results demonstrate that EAG2 promotes MB metastasis, a function distinct from its role in driving primary tumor growth."
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"We find that EAG2 channel is enriched at the trailing edge of migrating MB cells to regulate local cell volume dynamics thereby facilitating cell motility, and EAG2 knockdown impairs MB metastasis in a xenograft model."
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"The finding of elevated EAG2 expression in metastatic lesions raised the prospect that EAG2 may promote MB metastasis or tumor growth at the disseminated site."
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"We identified the FDA approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient."
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Thioridazine inhibits KCNH5.
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"It thus appears that thioridazine block of EAG2 potassium channel not only compromises its volume regulation crucial for human MB cell proliferation and motility, but also reduces the activity of KCNT2 potassium channel as a downstream effector of EAG2 channel activity (XREF_SUPPLEMENTARY)."
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"Thioridazine blocks EAG2 and reduces MB tumorigenicity."
Thioridazine activates KCNH5.
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"The similar effects of thioridazine, astemizole and EAG2 knockdown (XREF_FIG and XREF_FIG, and XREF_SUPPLEMENTARY) thus indicate that thioridazine reduces MB cell growth and motility by blocking EAG2 channels."
NOG affects KCNH5
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Transcriptionally active NOG decreases the amount of KCNH5. 3 / 3
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biopax:ctd
No evidence text available
biopax:ctd
No evidence text available
biopax:ctd
No evidence text available
Calcium(2+) affects KCNH5
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"Using immunoprecipitation with the prepared antibody conjugated beads, followed by immunoblot analysis with the same antibody, we examined if an increased Ca 2+ concentration might cause proteolytic cleavage of native EAG2 proteins."
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"A sustained increase in the intracellular Ca (2) + concentration induces proteolytic cleavage of EAG2 channel."
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"Besides EAG1, AA also activates EAG2 and ERG1 channels, implicating a conserved mechanism involved in AA-mediated activation of the EAG channel family [ xref , xref ]."
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"Besides EAG1, AA also activates EAG2 and ERG1 channels, implicating a conserved mechanism involved in AA mediated activation of the EAG channel family [XREF_BIBR, XREF_BIBR]."
KCNH5 affects KCN
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KCNH5 increases the amount of KCN.
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KCNH5 increases the amount of KCN. 1 / 1
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"The Eag1 and Eag2, voltage dependent potassium channels, and the small-conductance calcium activated potassium channel (Kcnn3) are highly expressed in limbic regions of the brain, where their function is still unknown."
KCNH5 activates KCN.
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KCNH5 activates KCN. 1 / 1
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"It thus appears that thioridazine block of EAG2 potassium channel not only compromises its volume regulation crucial for human MB cell proliferation and motility, but also reduces the activity of KCNT2 potassium channel as a downstream effector of EAG2 channel activity (XREF_SUPPLEMENTARY)."
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KCNH5 inhibits Cell Survival.
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"We provide evidence that the known EAG2 channel blocker astemizole reduces MB cell migratory polarization and cell rear contraction, and impairs MB cell viability, motility and allografted tumor growth (XREF_FIG and XREF_SUPPLEMENTARY)."
KCNH5 activates Cell Survival.
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"We demonstrate that pharmacological inhibition of EAG2 reduces MB cell viability and motility, and identify an FDA approved antipsychotic drug, thioridazine, as a novel EAG2 channel blocker with potent efficacy in reducing intracranial xenograft MB growth and metastasis."
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Transcriptionally active hsa-miR-5704 decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-5582-3p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-548o-3p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-514b-5p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-513c-5p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-4717-5p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-3926 decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-15a-3p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-1323 decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-1295b-3p decreases the amount of KCNH5. 1 / 1
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biopax:mirtarbase
No evidence text available
Dihydrogen affects KCNH5
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"We show here that Kv10.2, Kv12.2, and Kv12.3 are similarly inhibited by external protons, suggesting that high sensitivity to physiological pH changes is a general property of EAG superfamily channels."
Astemizole affects KCNH5
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"However, these residues do not seem to be involved in the block we describe here because hEag2 channels expressed in Xenopus oocytes were blocked indistinguishable from hEag1 channels by astemizole (IC 50 for both ~ 1.5 muM; unpublished data)."
ZC3HAV1 affects KCNH5
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ZC3HAV1 increases the amount of KCNH5. 1 / 1
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"Silencing of TRIM25, KCNH5, JAK1, and ZC3HAV1 led to increased virus replication for at least 2 of the 3 siRNAs (XREF_FIG), which was consistent with reduced protein levels of TRIM25 (XREF_SUPPLEMENTARY) and ZAP (XREF_SUPPLEMENTARY), and reduced mRNA levels of KCNH5 and JAK1 (XREF_SUPPLEMENTARY)."
TRIM25 affects KCNH5
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TRIM25 increases the amount of KCNH5. 1 / 1
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"Silencing of TRIM25, KCNH5, JAK1, and ZC3HAV1 led to increased virus replication for at least 2 of the 3 siRNAs (XREF_FIG), which was consistent with reduced protein levels of TRIM25 (XREF_SUPPLEMENTARY) and ZAP (XREF_SUPPLEMENTARY), and reduced mRNA levels of KCNH5 and JAK1 (XREF_SUPPLEMENTARY)."
MDL28170 affects KCNH5
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MDL28170 inhibits KCNH5. 1 / 1
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"Thus, MDL28170 at high concentrations prevented the cleavage of EAG2 proteins."
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"EAG2 localizes to the trailing membrane of migrating cells where it promotes local cell volume reduction, and enhances cell motility and tumor metastatic potential (XREF_FIG)."
KCNH5 affects cell growth
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"EAG2 knockdown not only impairs MB cell growth in vitro, but also reduces tumor burden in vivo and enhances survival in xenograft studies."
KCNH5 affects Protease
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"Bacillus subtilis EAG-2 strain isolated from an ornamental plant nursery produced a highly active extracellular protease."
KCNH5 affects JAK1
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KCNH5 increases the amount of JAK1. 1 / 1
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"Silencing of TRIM25, KCNH5, JAK1, and ZC3HAV1 led to increased virus replication for at least 2 of the 3 siRNAs (XREF_FIG), which was consistent with reduced protein levels of TRIM25 (XREF_SUPPLEMENTARY) and ZAP (XREF_SUPPLEMENTARY), and reduced mRNA levels of KCNH5 and JAK1 (XREF_SUPPLEMENTARY)."
KCNH5 affects IC 50 of ~1.5 muM 32
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KCNH5 inhibits IC 50 of ~1.5 muM 32. 1 / 1
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"Moreover, EAG2 knockdown markedly reduced the motility of MB cells without affecting directionality, as did the EAG2 channel blocker astemizole, a known EAG2 channel blocker with an IC 50 of ~ 1.5 muM 32 (XREF_FIG)."
KCNB2 affects KCNH5, and SNP
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KCNB2 binds KCNH5 and SNP. 1 / 1
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sparser
"By searching for two-way interactions in a panel of candidate genes implicated in memory, we observed an additive interaction between KCNB2 SNP rs7006287 and KCNH5 SNP rs243146."
JAK1 affects KCNH5
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JAK1 increases the amount of KCNH5. 1 / 1
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"Silencing of TRIM25, KCNH5, JAK1, and ZC3HAV1 led to increased virus replication for at least 2 of the 3 siRNAs (XREF_FIG), which was consistent with reduced protein levels of TRIM25 (XREF_SUPPLEMENTARY) and ZAP (XREF_SUPPLEMENTARY), and reduced mRNA levels of KCNH5 and JAK1 (XREF_SUPPLEMENTARY)."
CUL7 affects KCNH5
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CUL7 inhibits KCNH5. 1 / 1
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"We found that Cul7 over-expression also significantly decreased the protein level of rat Eag2 proteins (XREF_SUPPLEMENTARY)."
APC affects CCND2, and KCNH5
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CCND2 binds APC and KCNH5. 1 / 1
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"In the current study we found that methylation of a number of genes was significantly associated with histologic type; adenocarcinoma was associated with increased methylation of APC, CCND2, KCNH5, and RUNX, and squamous cell carcinoma was associated with increased methylation of CDKN2A. There were trends towards larger tumors being associated with increased methylation frequency."