当前位置: X-MOL 学术BMC Mol. Cell Biol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Dlx5 and Dlx6 can antagonize cell division at the G1/S checkpoint
BMC Molecular and Cell Biology ( IF 2.8 ) Pub Date : 2019-04-11 , DOI: 10.1186/s12860-019-0191-6
Rachel K. MacKenzie , Parvathy Ravi Sankar , Andrew J. Bendall

Dlx5 and Dlx6 stimulate differentiation of diverse progenitors during embryonic development. Their actions as pro-differentiation transcription factors includes the up-regulation of differentiation markers but the extent to which differentiation may also be stimulated by regulation of the cell cycle has not been addressed. We document that expression of Dlx5 and Dlx6 antagonizes cell proliferation in a variety of cell types without inducing apoptosis or promoting cell cycle exit. Rather, a variety of evidence indicates that elevated Dlx5 and Dlx6 expression reduces the proportion of cells in S phase and affects the length of the cell cycle. Antagonism of S-phase entry by Dlx5 and Dlx6 proteins likely represents a lineage-independent function to effect Dlx-mediated differentiation in multiple progenitor cell types.

中文翻译:

Dlx5和Dlx6可以拮抗G 1 / S检查点的细胞分裂

Dlx5和Dlx6刺激胚胎发育过程中多种祖细胞的分化。它们作为促分化转录因子的作用包括分化标志物的上调,但是还没有解决细胞周期调节也可能刺激分化的程度。我们证明了Dlx5和Dlx6的表达可拮抗多种细胞类型中的细胞增殖,而不会诱导细胞凋亡或促进细胞周期退出。相反,各种证据表明升高的Dlx5和Dlx6表达降低了S期细胞的比例并影响了细胞周期的长度。Dlx5和Dlx6蛋白对S期进入的拮抗作用可能代表了谱系独立功能,可在多种祖细胞类型中实现Dlx介导的分化。
更新日期:2019-04-11
down
wechat
bug