Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00614
[1], [2], [3]
RNA modification NEAT1 NEAT1 ADAR Methylation : modification sites Indirect Enhancement m6A modification hsa-miR-34a hsa-miR-34a METTL14 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 14 (METTL14) WRITER
m6A Target hsa-miR-34a
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 Nuclear paraspeckle assembly transcript 1 (NEAT1) View Details
Crosstalk Relationship A-to-I  →  m6A Enhancement
Crosstalk Mechanism RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary ADAR1 interacts with Nuclear paraspeckle assembly transcript 1 (NEAT1), increasing it's A-to-I level and promoting its physical interaction with hsa-miR-34a, which was regulated by METTL14-mediated m6A modification.
In-vitro Model
HUVEC-C Normal Homo sapiens CVCL_2959
References
Ref 1 Adenosine-to-inosine Alu RNA editing controls the stability of the pro-inflammatory long noncoding RNA NEAT1 in atherosclerotic cardiovascular disease. J Mol Cell Cardiol. 2021 Nov;160:111-120. doi: 10.1016/j.yjmcc.2021.07.005. Epub 2021 Jul 21.
Ref 2 N6-Methyladenosine Induced miR-34a-5p Promotes TNF-alpha-Induced Nucleus Pulposus Cell Senescence by Targeting SIRT1. Front Cell Dev Biol. 2021 Mar 5;9:642437. doi: 10.3389/fcell.2021.642437. eCollection 2021.
Ref 3 NEAT1 silencing alleviates pulmonary arterial smooth muscle cell migration and proliferation under hypoxia through regulation of miR?34a?5p/KLF4 in?vitro. Mol Med Rep. 2021 Nov;24(5):749. doi: 10.3892/mmr.2021.12389. Epub 2021 Sep 1.