What is Anti-E2F1?

Cell cycle regulation by a number of genes involved is a multi-step process that involves a variety of cytokines. Which, by the cyclin-dependent kinase (CDK4), cyclin (CyclinD1), retinoblastoma gene (Rb), multiple tumor suppressor gene (P16) and E2F regulation loop is composed of cell cycle regulation during a important cellular regulatory pathways. Under normal circumstances, CDK4 and Cyclin D1 binds to the Rb protein phosphorylation and inactivation, Anti-E2F1 release, positive regulation of cell proliferation cycle. P16 protein CyclinD1 competitive binding with CDK4 and make inactivated, preventing phosphorylation of Rb protein, thereby negatively regulate cell proliferation cycle. In many human malignancies, were found to have the abnormal pathway, P16 and Rb inactivation, inhibition of cell cycle regulation of E2F pathway weakened, E2F activation of enhancing DNA synthesis and cell division, the tumor cells were uncontrolled growth. This study aimed to investigate the cancer E2F-1 factor activity and cell cycle. 1 Materials and methods 1.1 Cell culture gastrointestinal cancer cell line HGC-27, BGC-823, SGC-7901, MKN45, MKN28, SH288, HT29, SW-620 purchased from the Chinese Academy of Sciences Institute of Cell Biology, RPMI-1640 culture.

Recent studies have found that, Anti-E2F1 unless involved in cell cycle regulation by p53-dependent and p53-dependent apoptosis in two ways, but in development and differentiation of hematopoietic cells is also play an important regulatory role. E2F1 knockout mice a significant proliferation of lymphocytes, but decreased tolerance and lead to lymphoma. Dendritic cells (DC) activation induces lymphocyte proliferation in E2F1 knockout mice whether E2F1 affects DC function, thereby causing the abnormal lymphocytes? Therefore, this research study focused on dendritic E2F1 cells and mechanisms of regulation. First, we found that in LPS-induced human peripheral blood monocyte-derived dendritic cells and murine dendritic cell line DC2.4 maturation, E2F1 gene transcription and protein expression have shown a transient decline. DC2.4 created using the knockdown or overexpression of E2F1 cells as a model and found that knocking down E2F1 can lead DC2.4 phenotype and function are mature. In contrast, high expression of E2F1 could significantly inhibit LPS-induced DC2.4 maturity. By E2F1 gene knockout mouse bone marrow derived DC phenotype testing to verify the above findings, suggesting that E2F1 plays for DC maturation feedback regulation.



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