Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05555
[1]
m6A modification hsa-miR-21-5p hsa-miR-21-5p METTL3 Methylation : m6A sites Direct Enhancement Non-coding RNA miR-21-5p SPRY1  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target hsa-miR-21-5p
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator hsa-miR-21-5p microRNA View Details
Regulated Target Sprouty RTK signaling antagonist 1 (SPRY1) View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary METTL3-m6A-miR-21-5p-Sprouty RTK signaling antagonist 1 (SPRY1)/ERK/NF-kB axis in obstructive renal fibrosis and provides a deeper understanding of renal fibrosis.
Responsed Disease Kidney disorders ICD-11: GB90
Pathway Response NF-kappa B signaling pathway hsa04064
Cell Process Inflammation
In-vitro Model
HK-2 [Human kidney] Normal Homo sapiens CVCL_0302
In-vivo Model Each mouse was anaesthetized with inhaled isoflurane, and the left proximal ureter was exposed. Then, the ureter was ligated with 6-0 silk thread and severed. In the sham operation group, the left ureters of mice were exposed, but not ligated or severed. The 3rd, 7th and 14th days after surgery were the time points for killing. At each time point, a total of 10 mice in the UUO group were executed, and a total of 10 mice in the sham group were also executed to serve as controls.
References
Ref 1 METTL3/N6-methyladenosine/ miR-21-5p promotes obstructive renal fibrosis by regulating inflammation through SPRY1/ERK/NF-KappaB pathway activation. J Cell Mol Med. 2021 Aug;25(16):7660-7674. doi: 10.1111/jcmm.16603. Epub 2021 Jun 24.