m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00161
 [1], [2], [3]
m6A modification ADAR1 ADAR1 METTL3 Methylation : m6A sites Direct Enhancement RNA modification HNF4A HNF4A ADAR Methylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
m6A Target Interferon-inducible protein 4 (ADAR1)
 Targert Gene 
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> Adenosine-to-Inosine editing (A-to-I)
Epigenetic Regulator Interferon-inducible protein 4 (ADAR1) WRITER View Details
Regulated Target Hepatocyte nuclear factor 4 alpha (HNF4A) View Details
Crosstalk Relationship m6A  →  A-to-I Enhancement
Crosstalk Mechanism m6A modification directly impacts RNA modification through modulating the expression level of RNA modification regulator
Crosstalk Summary METTL3 methylates Interferon-inducible protein 4 (ADAR1) mRNA, thereby enhancing its protein expression, which subsequently promotes ADAR mediated A-to-I RNA editing of the Hepatocyte nuclear factor 4 alpha (HNF4A) transcript.
Responsed Drug BI6015
 Drug Info 
Pathway Response mRNA surveillance pathway hsa03015
RNA degradation hsa03018
Cell Process RNA stability
In-vitro Model
 MGG8 Glioblastoma Homo sapiens CVCL_D1H4
U-87MG ATCC Glioblastoma Homo sapiens CVCL_0022
U-118MG Astrocytoma Homo sapiens CVCL_0633
HepaRG Hepatitis C infection Homo sapiens CVCL_9720
Full List of Potential Compound(s) Related to This m6A-centered Crosstalk
Hepatocyte nuclear factor 4 alpha (HNF4A) 3 Compound(s) Regulating the Target Click to Show/Hide the Full List
 Compound Name BI6015 Investigative [4]
Synonyms
BI 6015; BI-6015
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MOA Antagonist
External Link
CID: 3269393
TTD: D02RRY
 Compound Name Lauric Acid Investigative [5]
Synonyms
DODECANOIC ACID; 143-07-7; n-Dodecanoic acid; Dodecylic acid; Vulvic acid; Laurostearic acid; Dodecoic acid; Duodecylic acid; 1-Undecanecarboxylic acid; Aliphat No. 4; Neo-fat 12; C12 fatty acid; Ninol AA62 Extra; Wecoline 1295; Neo-fat 12-43; Hydrofol acid 1295; Hydrofol acid 1255; Duodecyclic acid; Hystrene 9512; Dodecylcarboxylate; Lauric acid (natural); Univol U-314; Lauric acid, pure; Coconut oil fatty acids; ABL; Undecane-1-carboxylic acid; Laurinsaeure; NSC-5026; CCRIS 669; C-1297; UNII-1160N9NU9U; n-Dodecanoate
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MOA Inhibitor
External Link
CID: 3893
TTD: D0N0UC
DrugBank: DB03017
 Compound Name MYRISTIC ACID Investigative [6]
Synonyms
Tetradecanoic acid; 544-63-8; n-Tetradecanoic acid; n-Tetradecoic acid; Crodacid; n-Tetradecan-1-oic acid; 1-Tridecanecarboxylic acid; Univol U 316S; Hydrofol acid 1495; Emery 655; Myristinsaeure; Myristate; tetradecoic acid; Hystrene 9014; Neo-fat 14; Myristic acid (natural); C14 fatty acid; Myristic acid, pure; n-Myristic acid; Tetradecanoate; acide tetradecanoique; NSC 5028; FEMA No. 2764; CCRIS 4724; CH3-[CH2]12-COOH; HSDB 5686; UNII-0I3V7S25AW; Philacid 1400; CHEBI:28875; AI3-15381; Prifac 2942; C14:0; EINECS 208-875-2
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MOA Inhibitor
External Link
CID: 11005
TTD: D08OBF
DrugBank: DB08231
References
Ref 1 N?-Methyladenosine Landscape of Glioma Stem-Like Cells: METTL3 Is Essential for the Expression of Actively Transcribed Genes and Sustenance of the Oncogenic Signaling. Genes (Basel). 2019 Feb 13;10(2):141. doi: 10.3390/genes10020141.
Ref 2 ADAR1 is a new target of METTL3 and plays a pro-oncogenic role in glioblastoma by an editing-independent mechanism. Genome Biol. 2021 Jan 28;22(1):51. doi: 10.1186/s13059-021-02271-9.
Ref 3 RNA Editing Enzymes Modulate the Expression of Hepatic CYP2B6, CYP2C8, and Other Cytochrome P450 Isoforms. Drug Metab Dispos. 2019 Jun;47(6):639-647. doi: 10.1124/dmd.119.086702. Epub 2019 Apr 15.
Ref 4 HNF4alpha antagonists discovered by a high-throughput screen for modulators of the human insulin promoter. Chem Biol. 2012 Jul 27;19(7):806-18.
Ref 5 How many drug targets are there Nat Rev Drug Discov. 2006 Dec;5(12):993-6.
Ref 6 The Protein Data Bank. Nucleic Acids Res. 2000 Jan 1;28(1):235-42. doi: 10.1093/nar/28.1.235.