Literature summary extracted from
Feng, Z.; Li, Q.; Meng, R.; Yi, B.; Xu, Q.
METTL3 regulates alternative splicing of MyD88 upon the lipopolysaccharide-induced inflammatory response in human dental pulp cells (2018), J. Cell. Mol. Med., 22, 2558-2568 .
Organism
EC Number |
Organism |
UniProt |
Comment |
Textmining |
---|
2.1.1.348 |
Homo sapiens |
Q86U44 and Q9HCE5 |
Q86U44 i.e. catalytic subunit METTL3, Q9HCE5 i.e non-catalytic subunit METTL14 |
- |
Source Tissue
EC Number |
Source Tissue |
Comment |
Organism |
Textmining |
---|
2.1.1.348 |
dental pulp |
levels of m6A and METTL3 are up-regulated in human dental pulp cells stimulated by lipopolysaccharide |
Homo sapiens |
- |
General Information
EC Number |
General Information |
Comment |
Organism |
---|
2.1.1.348 |
physiological function |
the levels of m6A and METTL3 are up-regulated in human dental pulp cells stimulated by lipopolysaccharide. METTL3 depletion decreases the expression of inflammatory cytokines and the phosphorylation of IKKalpha/beta, p65 and IkappaBalpha in the NF-kappaB signalling pathway as well as p38, ERK and JNK in the MAPK signalling pathway in lipopolysaccharide-induced dental pulp cells. The vast number of genes affected by METTL3 depletion is associated with the inflammatory response. METTL3 knockdown facilitates the expression of MyD88S, a splice variant of MyD88 that inhibits inflammatory cytokine production |
Homo sapiens |