论文部分内容阅读
全反式维甲酸(all-trans retinoic acid,at RA)可诱导缺乏内源p53基因的人白血病细胞HL-60的粒细胞分化,在此过程早期,人p21周期蛋白依赖激酶抑制因子(Cyclin-dependent Kinase interacting protein,Cipl)的表达即有所增加,并且不依赖p53。将反应p21Cipl重组质粒转染进HL-60细胞,建立锌调表达反义p21Cipl的细胞系HLAC,再用RA诱导,发现反义p21Cipl可部分抑制HL-60细胞的分化,而此时CDK4和cyclin D3的表达在HLAC中明显增加,证明p21Cipl参与了这一分化过程的起始,CDK4和cyclin D3可能与这一过程密切相关。
All-trans retinoic acid (at RA) induces granulocyte differentiation of human leukemia cell line HL-60, which lacks endogenous p53 gene. In the early stage of this process, human p21 cyclin-dependent kinase inhibitor (Cyclin- The expression of the dependent Kinase interacting protein (Cipl) is increased and does not depend on p53. The recombinant plasmid p21Cip1 was transfected into HL-60 cells to establish a zinc cell line expressing HLAC against p21Cip1. After induction with RA, it was found that antisense p21Cip1 partially inhibited the differentiation of HL-60 cells, and at this time, CDK4 and cyclin were detected. The expression of D3 was significantly increased in HLAC, demonstrating that p21Cipl is involved in the initiation of this differentiation process, and CDK4 and cyclin D3 may be closely related to this process.