Investigate the role of miR-328 in the cell affecting the activities targeting CD44 Antibody expression.

We studied the effects of anti-CD44 murine monoclonal antibodies on the activation of antigen-specific hybridoma T cell Anti-CD44 murine antibodies by themselves did not induce the production of IL-2 by antigen specific T cell hybridoma. However, Anti-CD44 murine monoclonal antibodies were able to inhibit or increase the production of IL-2, using other monoclonal antibodies used as comitogenic stimuli. When a T cell hybridoma was activated by antigen and antigen-presenting cells or anti-CD3, the addition of anti-CD44 inhibits the production of IL-2. In contrast, monoclonal anti-CD44 antibodies acted synergistically with anti-human CD2 by stimulating a murine T cell hybridoma stably transfected with human CD2 gene to produce IL-2. Therefore, the crosslinking of the surface of CD44 is able to deliver positive or negative signal in murine antigen-specific T cell hybridoma. One of the ligands for CD44 is hyaluronic acid. The hyaluronic acid in vitro significantly increased the activation of murine T cell hybridomas. Hyaluronic acid itself was mitogenic for T cell hybridomas Therefore, in addition to being an adhesion molecule. CD44 molecule acts as a signal transduction of murine T cell hybridomas.

In animals, miRNA genes are transcribed to generate long primary transcripts (called pri-miRNA), which are first cut by the RNase III enzyme Drosha to generate some type hairpin intermediate (called pre-miRNA ) in the nucleus. Pre-miRNAs are then exported to the cytoplasm by exportin-5, a member of the family of Ran-dependent transport of nuclear receptors. Following the arrival in the cytoplasm, pre-miRNAs are subjected to another processing step by Dicer, a cytoplasmic RNase III-type enzyme. Although miRNAs have emerged as key regulators of gene expression, our understanding of the specific roles of miRNAs has been limited because of difficulty following the functions of a particular miRNA. Exogenous miRNAs are easily degraded by enzymes, making it impossible to obtain stable cell lines expressing miRNA long-term in vitro or in vivo. Although the expression of a large fragment of DNA harboring the promoter and the sequence of microRNA (s) has a stable expression possible , in many cases microRNAs are expressed as a cluster, making difficult to distinguish the function of a particular microRNA. To enable long-term studies of miRNA function in vitro and in vivo, we developed an expression vector harboring two copies of pre-microRNAs, a monitoring unit and a GFP selectable marker antibiotic. This allows a high-level stable expression of miRNA in the cells of interest for functional studies and complementation. Using this technique, we successfully expressed a number of miRNAs in mammalian cells, including miR-328. Using the available software. we found that miR-328 potentially targets a number of cell adhesion molecules, including CD44. This study was designed to investigate the role of miR-328 in the cell affecting the activities targeting CD44 Antibody expression.

CD44 is a cell surface antigen that expresses the breath of leukemia of myeloid leukemia most acute (AML) patients. It was reported that the ligation of CD44 with some specific anti-CD44 monoclonal antibodies can reverse the blockage of differentiation of leukemia cell lines. In this study, the effects of differentiation and apoptosis inducing HI44a, another monoclonal anti-CD44 (IgG2a), were investigated on leukemia cells obtained from 31 patients with AML-M2, M3, LAM, LAM- AML-M4 or M5. When cells were treated with AML HI44a, the percentage of nitroblue tetrazolium (NBT) + cells was significantly increased. The expression of CD11b, CD14 and CD15 on treated AML cells was also increased compared to control AML cells. In addition, HI44a was found to induce apoptosis of leukemic cells, as evidenced by annexin-V test. The average percentage of apoptotic cells in the cells of LAM-treated HI44a was significantly increased compared to that in cells of AML monitoring. Moreover, the level of transcript expression of c-myc in AML cells was found to be clearly decreased in all patients detected. These results indicate that HI44a effectively induces both differentiation and apoptosis of AML cells and suggests that the activity of Anti-CD44 Antibody may be associated with its inhibitory effect on the expression of c-myc transcription.

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