液泡蛋白分选
生物
细胞生物学
基因敲除
内吞作用
细胞周期
胚胎干细胞
RNA干扰
转染
信号转导
细胞
基因
分子生物学
内体
遗传学
核糖核酸
细胞内
作者
Dan‐Na Chen,Fei He,Ting Lu,Jin Huang,Meiyi Li,Decheng Cai,Cheng Huang,Dong Chen,Fu Xiong
出处
期刊:Genesis
[Wiley]
日期:2021-03-07
卷期号:59 (4)
被引量:4
摘要
VPS4B (vacuolar protein sorting 4B), a member of the ATPase associated with diverse cellular activities (AAA) protein family, is a component of the endosomal sorting complexes required for transport machinery which regulates the internalization and lysosomal degradation of membrane proteins. We previously reported that VPS4B is one of the pathogenic genes related to dentin dysplasia type I, although its function was largely unknown. To investigate the role of VPS4B in tooth development, we deleted the Vps4b gene in mice. We found that heterozygous knockout mice (Vps4b+/- ) developed normally and were fertile. However, homozygous deletion of the Vps4b gene resulted in early embryonic lethality of Vps4b-/- mice at approximately embryonic day 9.5 (E9.5). To investigate the underlying molecular mechanisms, we examined the molecular functions of VPS4B in vivo and in vitro. Cell experiments showed that VPS4B influenced the proliferation, apoptosis, and cell cycle of transfected human neuroblastoma cells (IMR-32 cells) with over-expression or knockdown of VPS4B. Moreover, qRT-PCR detection showed that the mRNA expression levels of apoptosis-, cell cycle-, and endocytosis-related genes was significantly down or up-regulated in RNA interference-mediated knockdown of VPS4B in IMR-32 cells and Vps4b+/- E12.5 embryos. We accordingly speculated that signal transduction disorders of cell endocytosis are a contributing factor to the prenatal lethality of Vps4b-/- mice.
科研通智能强力驱动
Strongly Powered by AbleSci AI