Literature summary for 2.1.1.348 extracted from

Wu, Y.; Xie, L.; Wang, M.; Xiong, Q.; Guo, Y.; Liang, Y.; Li, J.; Sheng, R.; Deng, P.; Wang, Y.; Zheng, R.; Jiang, Y.; Ye, L.; Chen, Q.; Zhou, X.; Lin, S.; Yuan, Q.
Mettl3-mediated m6A RNA methylation regulates the fate of bone marrow mesenchymal stem cells and osteoporosis (2018), Nat. Commun., 9, 4772 .

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q8C3P7	-	-

Synonyms

Synonyms	Comment	Organism
METTL3	-	Mus musculus

General Information

General Information	Comment	Organism
malfunction	conditional knockout of the m6A methyltransferase Mettl3 in bone marrow mesenchymal stem cells induces pathological features of osteoporosis in mice. Mettl3 loss-of-function results in impaired bone formation, incompetent osteogenic differentiation potential and increased marrow adiposity. Knockout of Mettl3 reduces the translation efficiency of mesenchymal stem cell lineage allocator Pth1r, and disrupts the PTH-induced osteogenic and adipogenic responses in vivo	Mus musculus
physiological function	Mettl3-mediated m6A RNA methylation regulates the fate of bone marrow mesenchymal stem cells and osteoporosis. Mettl3 overexpression in mesenchymal stem cells protects the mice from estrogen deficiency-induced osteoporosis. Parathyroid hormone/Pth1r (parathyroid hormone receptor-1) signaling axis is an important downstream pathway for m6A regulation in mesenchymal stem cells	Mus musculus

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Release 2023.1 (January 2023)