Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification

Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification

Germline or somatic variation in the family of KMT2 lysine methyltransferases have been associated with a variety of congenital disorders and cancers. Notably, KMT2A-fusions are prevalent in 70% of infant leukaemias but fail to phenocopy short latency leukaemogenesis in mammalian models, suggesting...

Full description

Bibliographic Details
Main Authors: Shailendra Maurya, Wei Yang, Minori Tamai, Qiang Zhang, Petra Erdmann-Gilmore, Amelia Bystry, Fernanda Martins Rodrigues, Mark C. Valentine, Wing H Wong, Reid Townsend, Todd E. Druley
Format: Article
Language:English
Published: Taylor & Francis Group 2022-02-01
Series:Epigenetics
Subjects:
histone methyltransferases
development
gene expression
chromatin remodelling
hemogenic endothelium
pluripotency
mesoderm
Online Access:http://dx.doi.org/10.1080/15592294.2021.1954780

Internet

http://dx.doi.org/10.1080/15592294.2021.1954780

Similar Items