General Information of the m6A Target Gene (ID: M6ATAR00561)
Target Name Potassium voltage-gated channel subfamily H member 6 (KCNH6)
Synonyms
Ether-a-go-go-related gene potassium channel 2; ERG-2; Eag-related protein 2; Ether-a-go-go-related protein 2; hERG-2; hERG2; Voltage-gated potassium channel subunit Kv11.2
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Gene Name KCNH6
Chromosomal Location 17q23.3
Family Potassium channel family, H (Eag) (TC 1.A.1.20) subfamily, Kv11.2/KCNH6 sub-subfamily
Function
Pore-forming (alpha) subunit of voltage-gated potassium channel. Elicits a slowly activating, rectifying current (By similarity). Channel properties may be modulated by cAMP and subunit assembly.
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Gene ID 81033
Uniprot ID
KCNH6_HUMAN
HGNC ID
HGNC:18862
Ensembl Gene ID
ENSG00000173826
KEGG ID
hsa:81033
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
KCNH6 can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line Embryonic stem cells Mus musculus
Treatment: METTL3 knockout mESCs
Control: Wild type mESCs
GSE156481
Regulation
logFC: 1.67E+00
p-value: 2.01E-04
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between KCNH6 and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 4.49E+00 GSE60213
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Lowering m6A levels through silencing METTL3 suppresses the FMT process in vitro and in vivo. m6A modification regulates EMT by modulating the translation of Potassium voltage-gated channel subfamily H member 6 (KCNH6) mRNA in a YTHDF1-dependent manner. Manipulation of m6A modification through targeting METTL3 becomes a promising strategy for the treatment of idiopathic pulmonary fibrosis.
Target Regulation Up regulation
Responsed Disease Idiopathic pulmonary fibrosis ICD-11: CB03.4
In-vitro Model WI-38 Normal Homo sapiens CVCL_0579
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Animals were bred and housed in the pathogen-free facility of the Laboratory Animal Center of Shanghai General Hospital (Shanghai, China). All lungs were collected 4 weeks after BLM treatment for histology and further study. Lung microsections (5 uM) were applied to Masson's trichrome and Sirius red staining to visualize fibrotic lesions.
YTH domain-containing family protein 1 (YTHDF1) [READER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Lowering m6A levels through silencing METTL3 suppresses the FMT process in vitro and in vivo. m6A modification regulates EMT by modulating the translation of Potassium voltage-gated channel subfamily H member 6 (KCNH6) mRNA in a YTHDF1-dependent manner. Manipulation of m6A modification through targeting METTL3 becomes a promising strategy for the treatment of idiopathic pulmonary fibrosis.
Target Regulation Up regulation
Responsed Disease Idiopathic pulmonary fibrosis ICD-11: CB03.4
In-vitro Model WI-38 Normal Homo sapiens CVCL_0579
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Animals were bred and housed in the pathogen-free facility of the Laboratory Animal Center of Shanghai General Hospital (Shanghai, China). All lungs were collected 4 weeks after BLM treatment for histology and further study. Lung microsections (5 uM) were applied to Masson's trichrome and Sirius red staining to visualize fibrotic lesions.
Idiopathic interstitial pneumonitis [ICD-11: CB03]
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Lowering m6A levels through silencing METTL3 suppresses the FMT process in vitro and in vivo. m6A modification regulates EMT by modulating the translation of Potassium voltage-gated channel subfamily H member 6 (KCNH6) mRNA in a YTHDF1-dependent manner. Manipulation of m6A modification through targeting METTL3 becomes a promising strategy for the treatment of idiopathic pulmonary fibrosis.
Responsed Disease Idiopathic pulmonary fibrosis [ICD-11: CB03.4]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
In-vitro Model WI-38 Normal Homo sapiens CVCL_0579
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Animals were bred and housed in the pathogen-free facility of the Laboratory Animal Center of Shanghai General Hospital (Shanghai, China). All lungs were collected 4 weeks after BLM treatment for histology and further study. Lung microsections (5 uM) were applied to Masson's trichrome and Sirius red staining to visualize fibrotic lesions.
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary Lowering m6A levels through silencing METTL3 suppresses the FMT process in vitro and in vivo. m6A modification regulates EMT by modulating the translation of Potassium voltage-gated channel subfamily H member 6 (KCNH6) mRNA in a YTHDF1-dependent manner. Manipulation of m6A modification through targeting METTL3 becomes a promising strategy for the treatment of idiopathic pulmonary fibrosis.
Responsed Disease Idiopathic pulmonary fibrosis [ICD-11: CB03.4]
Target Regulator YTH domain-containing family protein 1 (YTHDF1) READER
Target Regulation Up regulation
In-vitro Model WI-38 Normal Homo sapiens CVCL_0579
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Animals were bred and housed in the pathogen-free facility of the Laboratory Animal Center of Shanghai General Hospital (Shanghai, China). All lungs were collected 4 weeks after BLM treatment for histology and further study. Lung microsections (5 uM) were applied to Masson's trichrome and Sirius red staining to visualize fibrotic lesions.
References
Ref 1 m(6)A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation. Mol Ther. 2021 Dec 1;29(12):3436-3448. doi: 10.1016/j.ymthe.2021.06.008. Epub 2021 Jun 8.