From: Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain
Title | Major findings | References |
---|---|---|
Developmental role of HMGN proteins in Xenopus laevis | Altered HMGN1 levels lead to malformations in Xenopus laevis development at the post-blastula stage | Körner et al. [178] |
High-mobility group proteins 14 and 17 maintain the timing of early embryonic development in the mouse | HMGN1 protein is necessary for the appropriate timing of embryo development in mice; depletion leads to developmental delays | Mohamed et al. [177] |
Binding of HMGN proteins to cell specific enhancers stabilizes cell identity | Loss of HMGN1 protein accelerates reprogramming of MEFs into iPSCs | He et al. [127] |
High mobility group nucleosome-binding family proteins promote astrocyte differentiation of neural precursor cells | HMGN1 expression promotes astrocyte differentiation | Nagao et al. [179] |
HMGN1 modulates nucleosome occupancy and DNase I hypersensitivity at the CpG island promoters of embryonic stem cells | Loss of HMGN1 reduces the number of Nestin-positive NPCs in SVZ in mouse brain | Deng et al. [129] |
Interplay between H1 and HMGN epigenetically regulates OLIG1 and 2 expression and oligodendrocyte differentiation | Loss of HMGN1 reduces OLIG1 and OLIG2 expression and impairs normal oligodendrocyte differentiation Loss of HMGN1 decreases the amount of MBP and proteolipid protein (PLP) in the spinal cord of mice | Deng et al. [124] |