Literature summary for 2.1.1.348 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 .

Search for more literature for 2.1.1.348

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q86U44 and Q9HCE5	Q86U44 i.e. catalytic subunit METTL3, Q9HCE5 i.e non-catalytic subunit METTL14	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
dental pulp	levels of m6A and METTL3 are up-regulated in human dental pulp cells stimulated by lipopolysaccharide	Homo sapiens	-

General Information

General Information	Comment	Organism
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

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Release 2023.1 (January 2023)