| First Author | Yang Y | Year | 2016 |
| Journal | Oncotarget | Volume | 7 |
| Issue | 14 | Pages | 17520-31 |
| PubMed ID | 27008703 | Mgi Jnum | J:278807 |
| Mgi Id | MGI:6359507 | Doi | 10.18632/oncotarget.8161 |
| Citation | Yang Y, et al. (2016) MiR-128-2 inhibits common lymphoid progenitors from developing into progenitor B cells. Oncotarget 7(14):17520-31 |
| abstractText | A considerable number of studies revealed that B cell development is finely regulated by transcription factors (TFs). Recent studies suggested that TFs are coordinated with microRNAs to control the development of B cells in numerous checkpoints. In the present study, we first found that miR-128-2 was differentially expressed in various immune organs and immunocytes. B cell development was inhibited in miR-128-2-overexpressed chimera and transgenic (TG) mice in bone marrow with decreased preproB, preB, proB, immature B, and recirculating B cells, as well as increased common lymphoid progenitors (CLPs). Further experiments showed that the apoptosis of CLP decreased, but proliferation was not altered in miR-128-2-overexpressed mice. Extensive studies suggested that the inhibition of apoptosis of CLP may be caused by miR-128-2 targeting A2B and MALT1, thereby increasing the phosphorylation of ERK and P38 MAPK. Such findings have prompted future investigations on the function of miR-128-2 in lymph genesis. |
