| First Author | Cheng L | Year | 2021 |
| Journal | Exp Cell Res | Volume | 398 |
| Issue | 1 | Pages | 112400 |
| PubMed ID | 33271126 | Mgi Jnum | J:302123 |
| Mgi Id | MGI:6503313 | Doi | 10.1016/j.yexcr.2020.112400 |
| Citation | Cheng L, et al. (2021) Loss of MBD2 affects early T cell development by inhibiting the WNT signaling pathway. Exp Cell Res 398(1):112400 |
| abstractText | DNA methylation alters the expression of certain genes without any alteration to the DNA sequence and is a dynamic process during normal hematopoietic differentiation. As an epigenetic regulator, methyl-CpG-binding domain protein 2 (MBD2) is an important member of the MBD protein family and is acknowledged as a "reader" of DNA methylation. We used a mouse model to study the effects of MBD2 on the early development of T cells. Here, we found that MBD2 deficiency led to retardation of T cell differentiation at the DN3 stage. Meanwhile, decreased proliferative capacity and increased apoptosis were detected in Mbd2(-/-) DN thymocytes. Furthermore, we found the WNT pathway was significantly down-regulated in Mbd2(-/-) DN thymocytes: DKK1 (Dickkopf-1) expression was significantly increased, while TCF7 (transcription factor 7) and c-MYC were down-regulated. Thus, these findings established that MBD2 acted as a dominant regulator to imprint DN T cell development via the WNT pathway. |
